Effects of Traffic Pollution on Risk of Autism and ADHD



Exposures of infants to toxins in vehicular traffic pollution during the first year after birth have been found to be strongly associated with risk of both autism and hyperactivity.  Close examination of the relevant studies on these topics provides strong implications about specific kinds of toxic exposures that originate from this pollution, exposures that can be greatly reduced by application of present-day knowledge on this topic.


There are some contradictions that become apparent when considering what seems to be a causal association between traffic pollution and these disorders.  Air pollution, including from vehicular traffic, has been declining in the U.S. during the same decades in which autism appears to have been increasing; and there seems to be no debate about whether substantial increases have taken place in ADHD in recent times, while traffic pollution has been declining.  So it may seem surprising that those disorders are associated with effects of this type of pollution.  But there is a perfectly logical explanation for this seeming contradiction, which will be presented in this paper.



Section A:  Autism strongly associated with postnatal traffic pollution, and linked far less with prenatal pollution.


Section B:  Components of traffic pollution that are known to be neurodevelopmental toxins, and why they have far greater effects after birth than before birth.


Section B.1:  PCBs, dioxins and PBDEs in traffic-related pollution

Section B.2:  Specifics about PCBs as developmental toxins in traffic-related pollution


Section B.3:  Specifics about PBDEs as developmental toxins in traffic-related pollution


Section B.4  Mercury in traffic-related pollution


Section C:  Other studies finding cognitive effects of postnatal exposures to traffic pollution


Section D:  Hyperactivity significantly associated with postnatal traffic pollution, but only among children of mothers with more than high school education.



Three surprising developments related to origins of autism and ADHD, and one logical explanation.


Section E:  Thoughts concerning the above







Section A:  Autism strongly associated with postnatal traffic pollution, and linked far less with prenatal pollution:


Notice in the chart below, from a review article,1 that odds of autism in association with high early-postnatal exposures to traffic-related air pollution were over three times as high as normal, dwarfing the equivalent odds for prenatal exposures. The research team (Volk et al., 2013) that found these outstandingly high odds for effects of early-postnatal exposures were authors or co-authors of over 850 published studies.

Fig. 1


Chart from Figure 2 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4855851 




A study in Israel,  published in 2018 (Raz et al.), also found statistically significant increased odds of ASD in relation to postnatal exposures to traffic-related air pollution, while finding no increased odds in relation to prenatal exposure.1c


So the question obviously comes up as to which of the many different components of traffic-related emissions might be causing increased autism.  There has been considerable research and speculation on this question, but so far most of it seems to have been centered around major components of air pollution (NO2, CO, etc.) that are not recognized developmental toxins.  Research regarding autism in relation to those components that are not known to be developmental toxins has yielded minimal-to-moderate associations; such associations could be found merely because those individual components co-vary with pollutants that are genuinely causal.  The highest odds ratios that appear to have been found for these typically-investigated individual components of traffic pollution have not even reached 1.75. (Figure 3 of above study)  That compares with the odds ratio associated with mixed traffic pollution of over 3.0; that high ratio applied to exposures during the year after birth  There is a strong implication that

   (a) toxins exist in the traffic pollution that are not being investigated and that are having more effects than the specific components that have been investigated so far, and

   (b) vulnerability of development to early postnatal exposures merits special attention.


Section B:  Specific components of traffic pollution that are known to be neurodevelopmental toxins, and why they have far greater effects postnatally than prenatally:


It would seem to be logical to look at least as much at vehicular pollution components that, although lower in volume than the ones that have been investigated so far, are known to be neurodevelopmental toxins.  A list of recognized developmental toxins, some of which are significant components of traffic-related air pollution, was provided in a 2016 scientific consensus statement; that statement (the TENDR statement) was signed by a group that includes 38 scientists and MD's, many of whom are highly-published authors of scientific studies.  It provides a list of six "prime examples of toxic chemicals that can contribute to learning, behavioral, or intellectual impairment."1a  Of the six chemicals on that list, three are very significant components of traffic-related air pollution:  PCBs, PBDEs, and mercury.  Another recognized developmental toxin that is very much a part of vehicular emissions and which is chemically related to PCBs and PBDEs is dioxin.


A publication of the EPA cites six studies, of both humans and animals, as indicating links between PCBs and ADHD; only one other toxin (lead) was mentioned as being implicated in relation to origins of ADHD.1b  There will be additional discussion below regarding PCBs, as well as about PBDEs and mercury, which were also included among the six toxins that the expert group specifically said can contribute to impairment.



Section B.1:  PCBs, dioxins and PBDEs in traffic-related pollution:   

In a 2013 U.S. study of PCB concentrations in carpet dust in homes at various distances from possible pollution sources, PCB concentrations were found to be about five times as high in homes within 600 yards from major roads in Los Angeles as they were in homes that were over 1100 yards from those roads;2 the p-value for this finding was <.01, indicating a high level of statistical significance.  In a study in Colombia, measurements of PCBs (as well as dioxins) taken near vehicular sources were found to be almost six times as high as measurements made over a mile farther away.4   In a study in Sweden, concentration of PCBs in ambient air pollution samples "decreased with increasing distance to the urban centre of Stockholm;" concentrations of each of the two basic types of PCBs declined more than 90% over the transition of sampling from urban center to outlying areas; the authors' focus in this sampling was on vehicular emissions, with their urban-center samples (with their highest PCB measurements) collected in two different road tunnels,68 where the pollution would be of distinctly vehicular origin.  The progressive decline in PCB content from those places to the outlying areas was very probably a result of declining density of and distance from vehicular traffic.


A publication of WHO points out that PCBs have been found to be about 1000 times as concentrated in urban air as in non-urban/non-industrial air.3  Given the above data about higher PCB levels near traffic, it is likely that traffic-related pollution was the largest contributor to that 1000-to-1 urban-to non-urban ratio. 


Specific types of PCBs that are known to be especially volatile3b are likely to comprise a large proportion of PCBs in traffic-related emissions suspended in nearby air; and some of those particular (lower-chlorinated) PCBs have been specifically reported to be active in neurotoxicity.3b


Research in Greece has found PCB emissions from gasoline-fueled vehicles to be far higher than PCB emissions from a number of other types of combustion that were measured. (See below.)

Fig. 1.a


(This chart accessed at https://www.researchgate.net/publication/7830615_Polychlorinated_in_ambient_air_of_NW_Greece_and_in_particulate_emissions_Environment_International_31_671-677 )


Many forms of combustion produce atmospheric PCBs, and gasoline-fueled vehicle emissions yielded by far the highest PCB concentrations among the various sources tested in the study that was the source of the above chart (Biterna et al.67). (Make note of the difference-obscuring effect of the log scale used in this chart.)


It is especially significant that the gasoline-fueled vehicle emission concentrations were found to be almost ten times as high as those of coal burning.  Consider the following:  In a publication of the European Environment Agency, the PCB emission factor for coal burning was itself shown to be high:  it was found to be within 10% of the emission factor for incineration of municipal wastes.67a  Municipal waste incineration would be expected to be an especially significant source of PCBs emitted to air, since that incineration typically includes input of discarded PCB-containing products  "as well as PCB formed in the process." 67b  According to a 2006 Korean study, "remarkably high concentration of PCBs in the flue gas of municipal solid waste incinerators and industrial waste incinerators, after conventional air pollution control measures, was reported in both Japan and Korea," citing three studies..67c  


Bringing together the above points:  Emission factors for PCBs from vehicles would be expected to be about 9 times as high as those from municipal incineration, which in themselves are important sources of PCB emissions.


Since PCBs have been found to be so substantially present in combustion emissions (especially traffic emissions), it should not be surprising that presence of at least one of the two major types of PCBs in air "correlates with population density," as found by EPA researchers.66b 



Dioxins:  A 2009 Czech study found "dramatic decreases" in concentrations of pollutants (including dioxins) in soil according to distances from roadways.  Concentrations next to roadways were found to be as high as in industrially-polluted areas.  Concentrations of dioxins were found to be continuing to decrease, stepwise, with progressive distances from roadways up to the last distance measured (100 meters); in measurements at four different locations at that distance, the concentrations were only 2% to 6% as high as next to the roadways.66h




As indicated above, average levels of PCBs and dioxins transferred to infants are generally far in excess of established safety standards, such that any extra contribution from exposure to traffic-related pollution would be a serious matter.



PBDEs, which are chemical relatives of PCBs and best known as intentionally-produced flame retardants, are similar to PCBs in being

   a) toxins that can cause impairment, on the TENDR list of the six of greatest concern,1a and

   b) produced by combustion, including in vehicle engines.


PBDEs appear to be produced in vehicle emissions in even greater amounts than PCBs,.  A Taiwanese study found that concentrations of PBDEs in vehicle exhausts were 17 to 140 times as high as concentrations of PCBs, in the different vehicles tested.6  (When reading that, remember from the first paragraphs of this section how high PCBs, themselves, have been found to be in vehicle emissions.)  In a 2010 study, the PBDE emission rate from tailpipe exhaust of just one unleaded-gas-fueled vehicle was found to be about four times higher than that from one U.S. house and garage.66d   (When reading that, bear in mind that U.S. houses, usually containing many flame-retardant-treated furnishings and electronics, are substantial sources of PBDE dust.66g)



PCBs and PBDEs in the environment last much longer during cold periods, which ties in with high autism rates in U.S. states with cold winters and areas of dense population.  The Biterna study found that PCB concentrations resulting from combustion emissions averaged 2.7 times as high during a cold period as during a warm period; bear in mind that this study was conducted in Greece, a southern European country.   A Finnish study found that half-lives of PBDEs' varied up to 200-fold according to season, lasting longest during the winter.66a


Given the above, it is very possible that areas of high vehicular traffic (mainly urban areas/ areas with high population density) make an unfavorable combination with cold winters, which greatly lengthen the lives of the developmental toxins emitted by the traffic. 


Considering that

a) both PCBs and PBDEs enter the air in substantial concentrations from vehicular traffic, which emits developmental toxins to which residents of cities would be most heavily exposed, and also that


b) both PCBs and PBDEs last many times longer in cold or winter conditions,



it should be of interest to look at any relevant child development data from unusually cold cities.  Consider the following:  18 of the 25 coldest U.S. cities with populations over 50,000 are located in the state of Minnesota.69  And Minnesota is reported to have by far the highest rate of autism in the entire U.S., according to the U.S. Department of Education.70  (see chart below)

Fig. 1.b




High rates of autism appear to be closely linked to proximity to high traffic combined with cold winters; high traffic in turn is related to urban location and population density.



But Minnesota's unique combination of much population density and very cold winters in correlation with outstandingly high autism prevalence is only the beginning of the associations along these lines. Correlation of autism prevalence with traffic-related toxins also pertains to other states among the cold, northern-most U.S. states --  especially Massachusetts and Maine.  For much more on this topic, related to these other states, see Appendix C.


The high levels of PCBs and PBDEs in vehicular emissions are very relevant to human development, as will be explained below.





Section B.2:  Specifics about PCBs as developmental toxins in traffic-related pollution: 


Readily absorbed from polluted air, and passed on to infants, in doses that could well be toxic:  According to the U.S. Agency for Toxic Substances and Disease Registry, "PCBs are readily absorbed through the gastrointestinal tract, respiratory system and skin," followed by distribution to and accumulation in adipose tissue.4a   PCBs are stored in breast milk fat,4d resulting in their being excreted in the milk during lactation.  The ATSDR document also points out, "Transfer of PCBs via breast milk can be considerable and, like prenatal exposure, has the potential to contribute to altered development." (p. 381)  


In studies published as of 2010, PCBs had been found to be present in human milk in doses 63 to 270 times the minimal risk level established by the U.S. ATSDR, according to the Oregon Department of Environmental Quality.4b  The studies on which the just-mentioned figures were based were probably not conducted specifically in high-traffic areas, so the average exceedance of the minimal risk levels would very likely be even higher for families living near major roads.

 Fig. 2


Infants are recognized to be vulnerable to these toxins in their early postnatal periods:  The early months after birth are a stage of high infant vulnerability to developmental toxins, according to the EPA, the ATSDR, the NIH, and the U.S. National Academies.4e  



In determining how likely an infant is to be significantly affected by PCBs from traffic emissions at this vulnerable stage, we need to consider the following matter:  There is considerable evidence about high versus low concentrations of PCBs taken in by infants depending on type of feeding received (see these charts as well as Sections 2.b and 3.a.2 at www.pollution-effects.info).  The greatly contrasting intakes of developmental toxins depending on feeding type (as indicated in these charts) could very well determine whether or not the infant's development is significantly harmed by the traffic-related toxins.  All infants would receive some direct exposure to the toxins by inhalation, more or less according to their distances from the roadways; but only breastfed infants would in addition receive greatly amplified exposures resulting from intakes by full-size bodies (mothers), intakes which become greatly concentrated in the process of being stored in fats and later mobilized and excreted in breast milk.8


Part of the evidence of PCBs' autism- and ADHD-related developmental toxicity:   According to the Washington State Department of Ecology, there is considerable evidence indicating that PCBs "impact normal brain development" and "are associated with ... deficits in IQ, memory, language and school performance” and lead to "chronic effects on a range of social and anxiety-related behaviors."  Based on a review of many studies related to effects of PCBs on development, an expert in this field summarized, "The general conclusion is that the higher the child’s exposure to PCBs in early life, the lower the IQ and the more the child exhibits anti-social behavior, depression, and attention deficit hyper-activity disorder-type symptoms."4c   (see Section 3.a of www.pollution-effects.info for much more on this topic)



Section B.3:  Specifics about PBDEs as developmental toxins in traffic-related pollution: 


Greatly amplified exposure to the traffic-related toxins due to breastfeeding: 

One study (by researchers who are authors of a total of over 740 studies) calculated that 91% of a typical U.S. breastfed infant’s total exposure to PBDEs was from breast milk.7  Assuming such a percentage, a maximum of 9% of an infant's PBDE exposure would normally come via all of the direct pathways, including inhalation of vehicle emissions; and ten times that amount would be transferred to the infant by an adult whose full-size body has taken in those same exposures. (A typical adult's intakes of PBDEs are recognized to be mostly from dust,9d, including traffic-related dust.)  That implies that a breastfed infant receives a ten-fold magnification of environmental exposures to PBDEs, which exposures would include those from vehicle emissions. 


When noting the above, remember from the earlier discussion of PBDEs that they have been found to be present in vehicle emissions in even higher concentrations than PCBs, and PCBs have in turn been found to be heavily present in vehicle emissions. (see Section B.1)


Another way of looking at the above:  Two experts on toxins involved in child development reported in 2006 that Persistent lipophilic substances, including specific pesticides and halogenated industrial compounds, such as PCBs (chemical relatives of PBDEs), accumulate in maternal adipose tissue and are passed on to the infant via breast milk, resulting in infant exposure that exceeds the mother’s own exposure by 100-fold on the basis of bodyweight. 8 


The concentrating effect of lactation in relation to PBDEs and their chemical relatives, PCBs and dioxins, has also been observed in many other studies.4e  Look at Figure 2 above and see what a breastfed infant's PCB levels would be expected to be like at five months of age, compared with the estimated PCB levels of a formula-fed infant at that same age.


Lactation also has an effect of concentrating mercury (one of the other components of traffic-related pollution), as found in the Chien et al. study.24


Fig. 3

image053.gifThere are many different "congeners" of PBDEs; but, as this chart (from  6) suggests, BDE 209 has been found to be by far the predominant congener in vehicular pollution.  See in the next several paragraphs about the EPA-recognized developmental toxicity of this traffic-related pollutant that becomes part of breast milk. The study that was the source of this chart focused on diesel emissions, but vehicular emissions in general have been found to be major sources of highly-brominated PBDEs such as BDE 209,10 including in deposits found in road dust.11  In what appears to be the only published data making the relevant comparisons, PBDE concentrations measured from the exhaust of gasoline-fueled vehicles were found to be about 60% higher than in emissions from diesel-fueled vehicles.6 



PBDEs neurodevelopmentally toxic if exposure is postnatal: 


There is considerable evidence on this topic, a small part of which is the EPA statement that “the most sensitive outcome of PBDE exposure is adverse neurobehavioral effects following exposure during the postnatal period."6a  


A 2012 study found that prenatal exposures to PBDEs had no significant adverse effects on children at age 4, but exposures via breastfeeding were associated with large increases in attention deficit problems and a 160% increased relative risk of poor social competence. (Notice two major traits that are core characteristics of autism and ADHD.)  Also in that same study it was found that lactational exposure to BDE 209, specifically, was associated with impaired cognitive development, and longer breastfeeding history was more strongly associated with neurodevelopmental impairment.14


To understand why prenatal exposures to certain chemicals should have no significant effect whereas postnatal exposures can have serious effects, note that (a) the placental barrier provides some protection to the fetus, (b) postnatal exposures are greatly amplified by the concentrating effect of breastfeeding (see "greatly amplifiied..." above), and (c) some sensitive stages of neurological development (including much development of the autism-related cerebellum) occur mainly or only during the months after birth.  See Sections 2.a, 2.b and 2.d of www.pollution-effects.info for detailed discussion of these topics.



In a 2014 document, the EPA rated 32 alternative flame retardants according to various characteristics, and BDE 209 was one of only three that received a "high" rating (the highest rating received) for developmental toxicity.15  Bear in mind that

-- a breastfed infant's exposure to PBDEs in general has been found to be overwhelmingly via breastfeeding,13


-- neurological impairment has been found to be associated specifically with BDE 209 in human milk, 17 and


-- the highly-developmentally-toxic BDE 209 has been found to be very strongly present in both traffic-related emissions (Fig. 3) and in breast milk (see just below).




Substantial presence of developmentally-toxic, traffic-related PBDEs, especially BDE 209, in human milk but not in infant formula:


According to data from Health Canada (a department of the Canadian government), an infant would be expected to ingest about 800 to 9000 times as much BDE 209 via breast milk as via infant formula.18  This toxin's high presence in human milk is at least partly explained by the fact that it accumulates in the body, as has been verified in multiple studies.19  Exposures of the mother to traffic pollution would take place over time, with the resulting accumulations being rapidly transferred to the infant in the early postnatal period; this is a period of high vulnerability to these toxins, according to the EPA and many other authoritative sources.20


A study found that concentrations of BDE 209 were over seven times as high in colostrum as in mature breast milk.14a This implies that the first few days of breastfeeding could be especially harmful.


Other types of PBDEs, also, have been found to be very low in infant formula, in contrast with the concentrations in human milk.14b



Section B.4:  Mercury in traffic-related pollution: 

Remember that methylmercury was one of the six environmental pollutants said in the TENDR statement1a to be especially likely to cause neuro-developmental harm, and is another one of those six that is known to be high in human milk.14c  Most other forms of mercury are also recognized to be neurologically toxic.



Mercury sediment has been associated with proximity to high traffic locations; all types of vehicles tested in multiple studies have been found to contribute to atmospheric mercury levels.21  An Indian study found atmospheric mercury to be even higher around traffic sites than the average reading taken around the industrial sites where measurements were taken.23


Elemental mercury from fuel combustion enters air, is readily absorbed by humans, and is eventually ingested by breastfed infants in concentrated form:


According to the U.S. ATSDR, "Approximately 80% of the mercury released from human activities is elemental mercury released to the air, primarily from fossil fuel combustion" and other human activities.23b  Also according to the ATSDR, "Inhalation is the primary route of exposure to elemental mercury vapor or aerosols, which are readily absorbed."23a   69% to 80% of inhaled elemental mercury vapor was found to be retained in human tissues, in the three studies cited by the ATSDR providing direct evidence on this topic. (p. 163 of 23b)  And the nervous system is considered to be the primary target organ for this form of mercury (p. 276 of 23b).  Elemental mercury is highly soluble in lipids (p. 331 of 23b); this makes it easily enter breast milk and be transported by it.  Bear in mind the Chien study that found infant exposure to mercury to be scores of times higher via breastfeeding than via inhalation.24


For much more about mercury, its recognized status as a neurodevelopmental toxin, and its adverse developmental effects after birth, see Section 3.d of www.pollution-effects.info


 Summarizing from above,


-- PCB residues have been found to be many times more concentrated near major roads than farther away;


-- PBDEs have been found in vehicular emissions in even higher concentrations than PCBs;


-- the specific type of PBDE (209) that is apparently the one that is most concentrated in vehicle emissions is considered by the EPA to be high in developmental toxicity; PBDEs in general have neurodevelopmental toxicity linked with effects that are similar to traits of autism;


-- good evidence indicates that postnatal, not prenatal, exposures to PCBs and PBDEs have the predominant toxic effects;


-- evidence of significant mercury pollution resulting from vehicular traffic has been found in multiple studies;


-- for all three of these toxins, the postnatal period is clearly a time of substantial developmental sensitivity; and


 -- an infant's postnatal exposures to all of the above chemicals from traffic-related pollution can become much higher as a result of breastfeeding, with lactation's effect of concentrating accumulated lipophilic chemicals.



Consider whether the combination of these factors could help explain the outstandingly high risk of autism that has been linked with traffic-related pollution specifically during the year after birth compared with minimal associations with prenatal exposures (as seen in Figure 1 above).


Much additional evidence about effects of exposures to these toxins will follow, especially about effects of exposures taking place during the year after birth.







Section C:  Other studies finding cognitive effects of mostly postnatal exposures to traffic and air pollution: 



In a study of urban Boston children 8–11 years of age, childhood exposure to black carbon (BC), a marker of traffic pollution, was associated with lower verbal IQ, nonverbal IQ, and visual memory abilities.  An interquartile-range increase in log black carbon predicted a 3-point decrease in IQ 47



A 2015 study found that children attending schools with higher levels of exposure to traffic-related air pollutants had a smaller growth in cognitive development over time.48 


In another Massachusetts study, in fully adjusted regression models, children with birth addresses within 50 meters (164 feet) of a major roadway were found to have lower mid-childhood nonverbal IQ scores (–7.5 points), verbal IQ scores (–3.8 points) and visual motor scores (–5.3 points) than participants living over 200 meters from a major roadway.  This is fully compatible with the critical exposure period's being postnatal.  Proximity of children’s homes to major roadways in mid-childhood appeared less strongly predictive of cognitive performance compared with time-of-birth exposures.49


A South Korean study measured exposures to air pollution during infancy, and almost 9,000 of those infants were followed up for a 10-year period.  Compared with infants with the lowest tertile of exposure to air pollution, those with the highest tertile (a one-third part) of pollution exposure had a 2-to-3-fold increased risk for ADHD.50


A 2015 article reviewing studies dealing with effects of air pollution summarized that air pollution exposure "in childhood has been inversely associated with neuro-developmental outcomes in younger children and with academic achievement and neurocognitive performance in older children.... the evidence as a whole suggests that vehicular pollution, at least, contributes to cognitive impairment."  The authors also noted that the studies "we have reviewed have been carried out on different populations, measured air pollution exposure in many different ways and have investigated many varying outcome measures...;"  and also, "Controlling for SES (socio-economic status) did not appear to substantially attenuate the associations."51


A 2016 review article summarized that "Recent epidemiologic studies in cities across the world provide convergent confirmatory evidence of the link between exposure to similar air pollution components, and (adverse) neurobehavioral outcomes....  In particular, vehicular emissions which are one important source of particulate pollution, have been associated with higher prevalence of frontal executive function deficits of preschool (2 to 5 year olds) and school aged children (6 to 14 year olds) in India, Boston, Cincinnati, New York City, China, Barcelona and Japan." 52

Fig. 4

pollutn&ASD.gifA 2015 study (Kalkbrenner et al.)53 explored sensitivity of early development to exposures to air pollution, during possible "windows of susceptibility," showing associations broken down according to three-month-periods before and after birth, in North Carolina and California.  In North Carolina, the numbers of cases studied were almost twice as large and the number of controls over five times as large as in California; therefore the data from North Carolina should carry greater weight overall.  Notice that the highest odds ratio (OR) for Autistic Disorder in this chart was for the first postnatal quarter in North Carolina, when breastfeeding would have been at its peak.  The only quarter with an odds ratio that approached that of the first postnatal quarter was Trimester 3; during that period, toxins would have been accumulating in maternal fat tissues, toxins that would later be mobilized and excreted in breast milk after birth, in concentrated form. (reference 8; also see Sections B.1 and B.2 above about PCBs and the highly-toxic BDE 209 accumulating in the body, and Section 3.a of www.pollution-effects.info for other supporting information)


Although the data for California was based on a far smaller sample, it was sufficient to reveal some relevant information. But before presenting that, we should indicate some important ways in which California, as a location for environmental factors that could lead to autism, is very different from North Carolina and other eastern U.S. states.


Fig. 5

California and North Carolina receive contrasting amounts of sun exposure; there are reasons to see that difference as leading to those states' having very different exposures to developmental toxins.


PCBs have been found to be degraded by UV light, and the degradation was observed to generally increase with UV intensity.66  PBDEs, also, especially the highly-brominated ones such as BDE 209, are degraded by light, as found in several studies;66f BDE 209 was found to decompose 50-300 times faster than the two other PBDE congeners  tested.66a (Remember from text next to Figure 3 the EPA-recognized especially high developmental toxicity of BDE 209 as well as its dominant presence in vehicular emissions.)  One study found that the PBDEs' half lives "varied among seasons up to 200-fold and had the longest half lives during winter."66a Consider the implications of those seasonal differences regarding rapid degrading of these toxins by heat and light; and consider what that means for the average levels of PCBs and PBDEs in air of sunny California versus the levels in North Carolina.

Fig. 5.a

Rainfall_U.S.2.jpgDifferences in rainfall between those two states are also great, and there are differences in exposures to mercury in traffic emissions that could be predicted to result from the differences in rainfall.  Remember from Section B.3 that elemental mercury resulting from fuel combustion enters air and is readily absorbed by humans. 

Those emissions typically rise and travel long distances and sometimes do not return to the earth's surface until a year or more after being emitted.  But they can also return to the surface quickly by the process called "washout"; this is one of the two major kinds of wet deposition of mercury,71 which in turn is "the primary method of removal of mercury from the atmosphere (approximately 66%)," according to the ATSDR. (p. 399 of 23b)  As opposed to "rainout" from clouds, washout can occur in lower-lying air, returning traffic-related mercury emissions to the same areas where the emissions originated.  If the mercury reaches the surface, "revolatilization" is a next step in "the bio-geochemical cycle of mercury."23c  So, as a result of precipitation, there would be additional inhalation by mothers and future mothers in the vicinity of the traffic-related pollution, as the mercury returns to the surface and as it rises again.  As mentioned earlier (Section B.3), most of inhaled mercury is absorbed into the body.


Therefore, when noting that traffic-related pollution in North Carolina seems to have a stronger, more rapidly-acting effect than similar pollution in California, we have to bear in mind the following:

 (a) mercury in the pollution can rise and drift far away, or

 (b) rain can keep it at human habitation/inhalation level very near its sources. 


Note in Figure 5.a above the differences between North Carolina and California in average rainfall and therefore in the comparative retention of traffic-related mercury near its sources.


PCBs, another of the developmental toxins concentrated in traffic-related pollution (see Section B.1) also return to the earth's surface in precipitation, and are also likely later to re-volatilize, according to the ATSDR53c and the NIH.23d  


Looking at Figure 5.a above, and considering how much (or how little) local washout of the toxins near roadways is likely to occur in those two different states, the reader should think about whether mothers' inhalation of air near roadways in California would lead to lower accumulations of toxins there than in North Carolina.


The climate differences would also be relevant to comparative vulnerabilities of development, in those two states.  A 2008 study (Waldman et al.) examined "the hypothesis that there is an environmental trigger for autism (that is) positively associated with precipitation," and the authors reported that their results supported this hypothesis.53a  Continuing, the Waldman et al. authors suggested, "Another possibility is that increased precipitation might promote weed growth or expansion of the insect population, which triggers an increased use of pesticides, which may serve as an environmental trigger for autism."  And there is very substantial evidence implicating pesticides as causes of autism and other neurological impairment.53b  The authors also pointed out the possibility that "vitamin D deficiency (resulting from insufficient exposure to sunlight) is an environmental trigger for autism.... Vitamin D deficiency can lead to reduced levels in the developing brain of calcitriol, a critical neurosteroid involved in brain development.  Of interest, while health care providers have exhorted patients during the last 20 years to reduce sunshine exposure, autism prevalence has been increasing...."65


So there are good reasons to conclude that (a) developmental toxins in the environment, which are probably entering human milk, could be much lower in California than in North Carolina, and that (b) children in sunny California could be less vulnerable to problems of neurological development than children in North Carolina.

Fig. 6         


Given the above, it should not be surprising that exposures to air pollution in California, as found in the Kalkbrenner et al. study, would not be linked with autism during the first two postnatal quarters. 


But notice the substantial increase in the third postnatal quarter.  By that time, even moderate exposures to toxins (continued long enough) may well have accumulated sufficiently in the infants to have reached high levels.  See below how an infant's levels of PCBs (much of which may have resulted from traffic emissions) build up with additional months of breastfeeding.  By the third quarter, additional exposures from the environment combined with the increasing accumulations from breastfeeding might be sufficient to tip the balance against healthy development.

PCBincrease_wBFing.gifFig. 7




These toxins accumulate in maternal fat (lipids), in maternal milk, and then in breastfed infants:


Bear in mind that developmental toxins discussed in this article (PCBs, PBDEs, and mercury) are known to the EPA to be bioaccumulative.53e 


a)  In infants:  In Figure 7 above/left, see estimated PCB levels accumulated in an infant breastfed for 10 months.

b)  In mothers:  "PBT (persistent, bioaccumulative and toxic) chemicals (including PCBs, PBDEs and mercury) partition from body lipids into breast milk because of its high lipid content," according to the U.S. ATSDR.61  A 1998 German study found that concentrations of mercury in breast milk of 85 lactating women at two months after birth had declined by an average of over 70% from their levels at time of birth,62 although some other studies have found a somewhat slower decline.  According to a 1999 Swedish study, “about 10% of the Hg (mercury) present in circulating blood would be transferred to the milk every day.”63  Different studies have estimated that concentrations of dioxins (chemical relatives of PCBs and PBDEs) in breast milk decline in the range of 48% to 70% during 6 months of breastfeeding.64


So transfers of a substantial part of the mother's accumulations would take place especially rapidly in the first quarter, possibly being sufficient at that time to have harmful effects, in an ordinary environment. But in a different environment in which toxins are degraded quickly (by sun exposure -- see text below Figure 5) or almost always blown away readily (due to minimal precipitation), the timing might be very different; it might take several months more before the accumulations (see Figure 7 above) could reach sufficiently high levels that, in combination with current exposures, developmental harm would result.  Length of time required before the scale can be tipped could also vary according to other health benefits of sun exposure in a specific environment, such as promotion of the vitamin D sufficiency that is critical to development of the brain, as mentioned above regarding California.



Effects of long-term exposures to developmental toxins, effects that would develop only with exposure that extends into the third postnatal quarter, would be especially likely to be realized in California:  The CDC's web page of breastfeeding data by states for 2010 shows that California had the highest long-term breastfeeding rates of all 50 U.S. states, in all three of the CDC's categories showing rates for breastfeeding for six months or longer; California's rate of exclusive breastfeeding through six months in 2010 was 54% higher than North Carolina's. 54


So we see what appear to be contrasting effects of developmental exposures to toxins in California versus those in North Carolina, with different postnatal periods in which development seems to be more vulnerable; the sensitive periods differ according to what could be predicted based on the contrasting climates of the two different states.  In an Eastern state with ample rain, considerable traffic-related pollution is retained at human level or rapidly returned to human level with precipitation; the toxins accumulate in breast milk, and development shows signs of being adversely affected soon after birth.  In a dry, very sunny Southwestern state, nursing mothers and infants have ample levels of Vitamin D, providing a good start for healthy neurological development; and levels of toxins in breast milk are probably below average, due to low deposition with rain and rapid degradation of toxins by sunlight; so developmental toxins in infants are likely to take longer to accumulate to harmful levels on average under such circumstances.  In addition, lactational transfer of toxins is far more likely to extend well into the third postnatal quarter in California;54 that means that the slower-growing accumulations in California could still be able to reach a developmentally-sensitive level, eventually; it would just be likely to take them longer to reach that level, as opposed to the rapid arrival that might take place in a state where toxin levels are higher.


Remember that, in the Kalkbrenner study, the authors were trying to identify "windows of susceptibility" when developing brains were most sensitive to toxins in the atmosphere.  In the cases of both states dealt with in that study, good evidence was found pointing to the postnatal period as the more sensitive period overall, even though the specific postnatal quarter of greatest sensitivity differed between states (see Figures 4 and 6); the period of greatest sensitivity probably varied according to effects of differences in climate and duration of breastfeeding, as discussed above.


However, the authors took those two very dissimilar data sets and merged them, and also added in data for the full, broad spectrum of  autism disorders; as might have been anticipated, the differences that  existed between the two focused data sets became unnoticeable in the amalgamation.  What the authors saw and reported about was what was most in common in the different data sets -- apparent effects of exposures during the third trimester of gestation.  As mentioned, the last months before birth are the time when maternal intakes of toxins, which would accumulate in fat tissues, would most accurately predict excretions in breast milk after birth.  The toxins accumulate, entering faster than they are being excreted; in addition to long-term accumulation, there are also short-term fluctuations according to varying intakes.  Major types of PBDEs have half lives in humans from two weeks to a few months,53g different forms of mercury have half lives in the body of 45 to 90 days,53m and PCBs have half-lives in the body ranging from a few months to many years.53f  So toxins to which the mother has increased exposure during the third trimester would accumulate and be present in the mother's body after birth, being excreted in breast milk especially during the first postnatal quarter.  But much of the prenatal maternal exposure would also remain longer, being more gradually excreted, being largely transferred to the infant over six or more months after birth


The U.S. ATSDR points out, in an understated way, that "the amount of PCBs transferred to offspring is expected to be higher during lactation than during gestation;" the magnitude of the difference is indicated by the "for example" that they provide in the next sentence:  "In female rats administered PCBs before gestation, an average of 0.003% of the administered dose was transferred to the fetus, whereas 5% was transferred to sucklings."53h  That works out to lactational transfer of PCBs that is about 1600 times greater than gestational transfer.  The ATSDR would not have provided that example without having good reason to see its relevance to humans.  Like the experimental animals, humans have placentas that provide protection to fetuses, certain toxins accumulate in maternal fat tissue (of both mammalian species), and those toxins are later mobilized and excreted during lactation.8


There is also relevant data available based directly on study of humans.  As stated in a publication of the National Academies Press, describing studies measuring maternal concentrations of developmental toxins in 313 women in Michigan, “The mean concentrations of PCBs were ... 3 ng/mL in cord serum, and 841 ng/g in breast milk.”53j (1 mL is about the same as 1 g when discussing a substance whose weight is about the same as that of water.)  That greater PCB concentration in each gram of breast milk could lead to a total infant exposure multiple that would be even higher than the 841 to 3 ratio, depending on how long the breastfeeding continues. (Remember, from text next to Figure 7, about PCBs' and other toxins' accumulating in the body.)  A 1600-times greater total lactational exposure to PCBs, compared with prenatal exposure (as found in rats under laboratory examination -- see above), may well be a valid indication of what also happens in humans when breastfeeding is continued for an average period.  But when breastfeeding continues for longer than average, it may lead to a total lactational exposure increase that is even greater than 1600 to 1.


Apparently many researchers (such as in the case of Kalkbrenner et al., above) look at times of elevated maternal intake of toxins and find associations between prenatal times of those increases and greater likelihood of the offspring's cognitive impairment as observed many years later; they then see that as evidence suggesting prenatal effects on the fetus.  But, as indicated earlier, that is not a valid inference.  The prenatal intakes are when toxins enter the mother, from where they are channeled mostly to storage in maternal fats;  part or all of those stored contents will, after birth, become part of a breastfed infant's food.  The maternal intakes are prenatal, but that says nothing about when (or whether) the developing fetus/infant will receive those toxins.  That is an extremely important point, bringing up the consideration of how transfer of toxins to a developing infant might be interrupted.


A 2011 study (by Mocarelli and 12 others)60 sheds some relevant light on what is probably happening in circumstances such as these.  There were accidental exposures in Seveso, Italy, to dioxins, a chemical relative of PCBs and PBDEs.  The study measured characteristics of sons of mothers who had been exposed to increased levels of dioxins before their sons’ births, resulting in what the authors called “modest elevations” of the mothers’ dioxin levels.  When the sons’ sperm quality and hormone concentrations were examined at ages 18 to 26, those who had been breastfed -- and only those who had been breastfed -- showed seriously adverse effects in all of the four different reproduction-related areas that were measured; by contrast, those who had been formula-fed showed no effects.  


If this study had been carried out in the way that the vast majority of studies are carried out, breastfeeding history -- and the link of adverse effects with breastfeeding history -- would have been ignored.  The results would ordinarily have been reported simply as showing that "prenatal" exposures to the dioxins were linked with the adverse outcomes. And the popular notion about the overwhelming importance of prenatal exposures would have received further reinforcement.  Such reinforcement would probably have been no more misguided than much or most of the other reinforcement that has been supporting this belief.


The reader should remember from above,

a) the 5- to-6-fold increase in PCB deposits near major roads,

b) the apparently still greater concentrations of (chemically-related) PBDEs in vehicular exhaust, compared with concentrations of PCBs;

c) the efficient absorption of these toxins, plus mercury (as also found in vehicular emissions), via inhalation; and

d) the fact that all of those toxins that are present in traffic pollution are known to have adverse effects on postnatal neurological development.53k


Then one should think about the likely 1600-times greater exposures received by lactation-fed infant animals after birth, following the mother's prenatal exposure to PCBs, as found under laboratory conditions;

and then consider how likely it is that developmental harm caused by those exposures takes place before birth, as would be suggested by many researchers.



Fig. 8


Data from this 2015 study (Talbott et al.55) provides still more support for a generalization of greater effects of environmental toxins on cognitive development postnatally, compared with prenatally.


It may seem surprising to see a somewhat higher odds ratio for year 2 than for year 1, considering the higher percentage of mothers who breastfeed (with accompanying transfer of developmental toxins) during year 1.  But the reader should note that (a) given the 95% confidence intervals (CIs) shown, the true relationship could very well be reversed, (b) PCBs and mercury are both known to often have delayed effects,57 and (c) in Pennsylvania where the study was carried out, 25% of mothers breastfeed for at least 12 months;54 on the likely assumption that a significant percentage of those long-term breastfeeders would continue past 12 months, that would be a very large number of mothers transferring traffic-related developmental toxins to their infants into the second year (see Section B), with the additional exposures going even farther past established safe levels than they already were after one year of nursing.(see Figure 7),



Section D:  Hyperactivity significantly associated with postnatal traffic pollution, but only among children of mothers with more than high school education; a mystery with a well-substantiated solution



As indicated in the above studies, there has already been strong evidence found for an association between exposure to traffic pollution and cognitive impairment.  A 2013 study (Newman et al.25) observed the same general association but with a substantial, very meaningful twist.  After studying children who had been exposed to an air pollution component that is a marker for traffic emissions (ECAT), the authors observed that elevated exposure during the child’s first year of life was significantly associated with hyperactivity scores in the “at risk” range at age seven.  But more significantly, the authors found a far stronger association in children whose mothers had higher education (aOR=2.3).  By contrast, there was no association related to traffic pollution among children of mothers who had no more than high school education. 


Notice that long-term breastfeeding rates of college graduates are about twice those of high-school graduates. (For supporting data from the CDC, see also 59)

 Fig. 9


The greater percentage of breastfeeding by mothers with higher education reflects only part of the extra exposure of their infants.  Several studies have found that "maternal education was the strongest predictor of breastfeeding exclusivity." 59b  Greater intensiveness (exclusivity) of breastfeeding, combined with a doubled percentage of breastfeeding among college graduates, could well mean that babies of college graduates would receive several times the effective exposure to any toxins contained in human milk, compared with babies of high school graduates.


As explained in Section B, certain developmental toxins (PCBs, PBDEs and mercury) are substantially present in traffic-related emissions, and they are well absorbed by inhalation; those traffic-related toxins accumulate in fatty tissues and are excreted in breast milk. (Section B.2)  PCBs and PBDEs are the kinds of toxins that experts quoted earlier were referring to when saying, Persistent lipophilic substances ... accumulate in maternal adipose tissue and are passed on to the infant via breast milk, resulting in infant exposure that exceeds the mother’s own exposure by 100-fold on the basis of bodyweight.8 


Given the above, should the following finding from the Newman study be surprising?:   that children of college graduates, with their high rates of breastfeeding and exclusivity of breastfeeding, are very significantly affected by traffic-related pollutants, whereas children of high-school graduates are not significantly affected.




Three of the studies described earlier (Newman et al. just above and Volk et al. 2013 and Raz et al. 2018 in Section A) are of particular interest with regard to cognitive effects of specifically postnatal exposures to traffic-related pollution.  Those studies include several surprising findings related to origins of autism and ADHD, which follow:


  -- a) Volk et al. and Raz et al. were especially significant in finding substantially higher adverse effects of traffic pollution specifically in the year after birth. There exists a widely-held notion that postnatal toxic exposures have low effects compared with prenatal exposures (even though there is ample evidence refuting that belief -- see www.disability-origins.info); so these findings of greater postnatal effects of traffic-related pollution merit special attention because of their conflicting with common expectations.

  -- b) ASD or ADHD was found in these three studies to be associated with a type of pollution that (according to the EPA -- see below) has been declining -- while ASD and ADHD have apparently been increasing.

Fig. 9.a



(Notice above that toxic emissions from on-road vehicles, shown by the dark red bands, have been determined to be declining at every point measured.)




-- c) The Newman et al. study was especially of interest in finding that traffic exposures during that vulnerable first year of life were associated with either strong adverse effects or no effects, depending on the mother's educational level.  Also surprising:  First bear in mind that children of mothers with higher education would normally have higher incomes and be able to afford to live farther from the emission sources, and children of mothers with less education would be more likely to live closer to urban traffic.58  But substantial adverse effects of traffic-related pollution were found among mothers who on average live farther from the pollution; and no effects of the pollution were found among the mothers who would usually live closer to the pollution.  So traffic-related pollution is found to have adverse effects, but not on the children who would be expected to have the greatest exposures to the pollution.  This appears to be a contradiction.


There is clearly a need for explanations that could apply to each of the above. 


As it turns out, there is a single explanation that would apply to all of the above, which will be described below.  This explanation is supported by substantial evidence, but it has the disadvantage of being politically incorrect, at odds with beliefs that have been popular in recent decades. 


Environmental toxins, including ones that are substantially present in traffic-related pollution, are recognized to become concentrated in human milk, as indicated in authoritative expert statements and many studies (Section B earlier and also references 8, 9); and these subsequent doses via lactation dramatically amplify the exposures to environmental toxins compared with exposures that are received directly. (see Sections B.3 and B.4)  It is also well established that the early months after birth (when breastfeeding is most active) are a time of considerable vulnerability of neurological development to environmental toxins.9b  Finally, infants have been exposed to this pathway for environmental toxins at greatly increased rates in recent decades, in most countries. (see Fig. 11 later about U.S. trends and below about many other countries)

Fig. 10


A major role for breastfeeding in origins of cognitive impairment, by way of transferring developmental toxins to infants at a time of infant vulnerability, is compatible with many other studies that have found associations between breastfeeding and risk of autism, including in dose-response relationships.  Among those are the following:


A 2011 study that investigated data from all 50 U.S. states and 51 U.S. counties found that "exclusive breast-feeding shows a direct epidemiological relationship to autism," and also, "the longer the duration of exclusive breast-feeding, the greater the correlation with autism." 39



Note that, according to the EPA, Epidemiologic studies of exposed human populations provide the most convincing evidence of human health effects.”43  Also, a dose-response relationship between an exposure and a health outcome is considered to be especially significant evidence to support a finding of cause and effect.  One example of a dose-response relationship, as found in a study by a well-published scientist (R.J. Shamberger), was quoted in the previous paragraph.  This finding was even more significant in that it was based on investigation of a very large, diversely-populated geographic area (all 50 U.S. states), and it also applied in relation to numerous smaller-scale units (51 counties). 


Additional support for a causal connection between breastfeeding and autism was provided by three additional, relatively recent studies, with a dose-response relationship being apparent in the different degrees of correlation with autism according to the different durations of breastfeeding, when these three studies are seen together.

-- In a 2011 Canadian study of a population of over 125,000, using discharge from the hospital as the dividing line for breastfeeding exposure, there was a 25% higher autism rate among the breastfed children than among non-breastfed children.40

-- In a 2009 U.K. study, the duration of breastfeeding that was assessed was four weeks versus less than that, with 65% of the autism cases having received breastfeeding for at least four weeks; that should be compared with only about 28% of the general U.K. infant population (where breastfeeding rates are relatively low) receiving that much breastfeeding; that meant a 130% higher-than-average likelihood of that much breastfeeding history among those with autism. 41

-- In a 2010 American study in Kentucky by two MD’s, the duration of breastfeeding used for comparison was six months, and 37% of autism cases had received that much breastfeeding, compared with 13% of the controls, indicating an approximately 185% (37%/13%) greater likelihood that the autism cases would have had more breastfeeding; the p-value was .003, meaning three chances out of a thousand that the finding was a result of chance occurrence.42


For more studies that have found positive links between breastfeeding and autism, see Section 4.a.2 of www.pollution-effects.info.



Section E:  Thoughts concerning the above:


It would seem that a finding of greatly increased risk of autism, reasonably connected with known exposures to recognized developmental toxins, should deserve close attention, especially since something can be easily done to drastically reduce the implicated exposures.  If a specific type of infant feeding is observed to concentrate and channel recognized developmental toxins to infants at a time of high vulnerability of the infants, that would seem to be very significant; especially if that feeding type could be replaced by one that was apparently quite satisfactory for nourishing the generation that was born in the mid-20th century.  Bear in mind that the U.S. mid-20th-century generation did not have the many epidemics and increases of non-communicable disorders that have become prevalent since then. (see below)



A viable alternative to breastfeeding:

Note that an alternative type of infant feeding is readily available that


(a) compared with human milk, contains less than 7% (and usually less than 1%) as much of the developmental toxins mentioned above (see Section 3.g of www.pollution-effects.info), and


(b) was the standard feeding type for the generation born in the U.S. “throughout the mid-20th century,” as stated by the American Academy of Family Physicians.26  According to what appears to be the most thorough study of infant feeding patterns in the U.S., breastfeeding declined until 1960, and “since the middle 1960s there has been a steady increase in the practice of breastfeeding in the US.”27  This is compatible with the historical charts below.

 Fig. 11


Remember that childhood disabilities and disorders, which by now have reached high levels, were reported to have first started emerging as major chronic conditions in the 1960’s, followed by more substantial increases beginning in the 1970’s and later (see Section 1 of www.pollution-effects.info).  Even flat breastfeeding rates (in 1962-1965, following earlier declines -- see Figure 11 above) would have been instrumental in an increasing transfer of developmental toxins to infants, considering that an increase of toxins in the environment (and therefore in human milk) had already begun in the 1940's and 1950’s.28


The generation that was seldom breastfed did not have childhood health problems on the scale that was to become commonplace after breastfeeding rates increased greatly. Evidence to support that statement (in addition to what was already presented in Section 1 at the above link) includes the following: 


Trend of chronic childhood health conditions since the 1960's, while breastfeeding was increasing:  According to a 2007 article in the Journal of the American Medical Association, “the number of children and youth in the United States with chronic health conditions…has increased dramatically in the past 4 decades.”  The authors referred to various studies finding very large increases in obesity (almost quadrupling in U.S. children between the early 1970’s and 2004), disability associated with childhood asthma (tripling between 1969 and the mid-1990s), and activity limitations due to a health condition of more than 3 months’ duration (quadrupling between 1960 and 2004). The authors predicted that “the expanding epidemics of child and adolescent chronic health conditions will likely lead to major increases in disability among young and then older adults in the next several decades.29


Studies in the New England Journal of Medicine and the Journal of Allergy and Clinical Immunology point to the 1970’s as the beginning of doubling and tripling of allergy rates, especially among children and young people.30  There is also ample evidence pointing to the 1970’s as the time when major increases in childhood diabetes began.31 Evidence also indicates that ADHD grew from low single digits to over 14% of U.S. boys over age 7 during the last few decades.32






Hypotheses about effects of NO2, CO, etc, in traffic-related pollution center around pollutants that are not recognized developmental toxins; and (perhaps not surprisingly) the risk ratios associated with those pollutants have been found to be comparatively minimal, at levels that are very compatible with those substances' having no causal effect on autism risk.  In any case, greatly reducing most of those pollutants in vehicle emissions would be difficult or impossible.  But it would be relatively easy to greatly reduce infants' exposures to known developmental toxins that originate from vehicular traffic, accumulate in women's bodies, and are later transferred in concentrated form to infants via lactation.




There was one especially noteworthy finding summarized in the study that was the source of the earlier chart (Figure 1) about traffic-related pollution exposures and odds of autism:  The odds of autism in relation to the pollution, as shown in Figure 2 of that study, were far lower for diesel pollution than for mixed-traffic pollution.1  That brings to mind comparisons that have been made of the two main kinds of vehicular pollution with regard to their contents of mercury.  A 2007 U.S. study, partly supported by the EPA, found that total mercury content in gasoline was 4.5 times the mercury content in diesel fuel.34  Another 2007 study found mercury content of gasoline to be over three times as high as mercury content of diesel fuel.35  A 2005 study in the San Francisco area found results similar to the above.  And remember from earlier that PBDE concentrations in gasoline emissions were found to be 60% higher than in diesel emissions.12


So the far higher levels of at least two recognized developmental toxins in gasoline than in diesel fuel (and/or in their emissions) may explain why adverse developmental effects of mixed traffic pollution have been found to be significantly higher than effects from diesel pollution.  This should be considered along with the substantial evidence suggesting that exposures to those two toxins (PBDEs and mercury) lead to higher risk of autism (see Sections 3.b and 3.d of www.pollution-effects.info).  Possibly more significantly, the fact that both of those toxins are present in human milk in many times higher concentrations than in infant formula (see above-linked sections) has an important implication:  exposures of infants to developmental toxins in traffic-related pollution (inhaled by mothers and excreted to breastfeeding infants) could be sharply reduced by mothers' no longer breastfeeding if they live near major roads.




Most studies have been assessing only prenatal exposures, in conformity with the widely-held notion that postnatal exposures do not have significant harmful effects on neurological development.  (To be more precise, they have said that they were assessing prenatal exposures, when they found associations with adverse effects, even though their measurements were typically taken at time of birth or later -- often in breast milk -- measurements that could in actuality be good indications of exposure via nursing.)  For many reasons as explained in Section 2 of www.pollution-effects.info, the belief in lack of significance of postnatal toxic exposures is mistaken, and it contributes to frequent failure to see the real causes of cognitive and other impairments.  The Volk et al. 2013 study, results of which are shown above (Figure 1),  the Newman et al. 2013 study, and the Kalkbrenner and Talbott studies make up a group that has apparently been distinctive in the following respects:   the only studies published as of January, 2017 in which neurological effects were investigated related to early-postnatal times of exposure to substantial mixed-traffic-related air pollution.38  The increased odds ratios for cognitive impairment in relation to postnatal exposures to traffic-related pollution, as found in all four of those studies, merit close attention.  Other studies in Section C are compatible with those studies in finding either postnatal sensitivity, or what could very well be postnatal sensitivity, to toxins contained in traffic-related pollution.  All of them illustrate the kind of thing that is typically not reported properly in many studies:  strongly-supported links of impairment with postnatal exposures to pollutants.  Those very real associations are not observed or reported because (a) the researchers simply do not look for them or (b) they measure exposures that are quite likely to actually reflect postnatal exposures (measured at time of birth or in breast milk) and then simple-mindedly call them "prenatal" exposures, when associating them with adverse outcomes.


In the search for solutions to major public health problems, an especially serious turn away from a useful path occurs when funding sources waste money on research that fails to look at easily-investigated, modifiable, likely postnatal sources of harmful exposures; even just asking for approximate duration of the child's breastfeeding could provide considerable useful information.





About the author:

As the author of the above, my role has not been to carry out original research, but instead it has been to read through very large amounts of scientific research that has already been completed on the subjects of environmental toxins and infant development, and then to summarize the relevant findings; my aim has been to put this information into a form that enables readers to make better-informed decisions related to these matters.  The original research articles and government reports on this subject (my sources) are extremely numerous, often very lengthy, and are usually written in a form and stored in locations such that the general public is normally unable to learn from them. 


My main qualification for writing these publications is ability to find and pull together large amounts of scientific evidence from authoritative sources and to condense the most significant parts into a form that is reasonably understandable to the general public and also sufficiently accurate as to be useful to interested professionals.  My educational background included challenging courses in biology and chemistry in which I did very well, but at least as important has been an ability to correctly summarize in plain English large amounts of scientific material.  I scored in the top one percent in standardized tests in high school, graduated cum laude from Oberlin College, and stood in the top third of my class at Harvard Business School.  


There were important aspects of the business school case-study method that have been helpful in making my work more useful than much or most of what has been written on this subject, as follows:   After carefully studying large amounts of printed matter on a subject, one is expected to come up with well-considered recommendations that can be defended against criticisms from all directions.  The expected criticisms ingrain the habits of (a) maintaining accuracy in what one says, and (b) not making recommendations unless one can support them with good evidence and logical reasoning.  Established policies receive little respect if they can’t be well supported as part of a free give-and-take of conflicting evidence and reasoning.  That approach is especially relevant to the position statements on breastfeeding of the American Academy of Pediatrics and the American Academy of Family Physicians, which statements cite only evidence that has been

   (a) selected, while in no way acknowledging the considerable contrary evidence,a1 and

   (b) of a kind that has been authoritatively determined to be of low quality. a1a -  a2c


When a brief summary of material that conflicts with their breastfeeding positions is repeatedly presented to the physicians’ associations, along with a question or two about the basis for their breastfeeding recommendations, those associations never respond.  That says a great deal about how well their positions on breastfeeding can stand up to scrutiny.


The credibility of the contents of the above article is based on the authoritative sources that are referred to in the footnotes:  The sources are mainly U.S. government health-related agencies and reputable academic researchers (typically highly-published authors) writing in peer-reviewed journals; those sources are essentially always referred to in footnotes that follow anything that is said in the text that is not common knowledge.  In most cases a link is provided that allows easy referral to the original source(s) of the information.  If there is not a working link, you can normally use your cursor to select a non-working link or the title of the document, then copy it (control - c usually does that), then “paste” it (control - v) into an open slot at the top of your browser, for taking you to the website where the original, authoritative source of the information can be found.  


The reader is strongly encouraged to check the source(s) regarding anything he or she reads here that seems to be questionable, and to notify me of anything said in the text that does not seem to accurately represent what was said by the original source.  Write to dm@pollutionaction.org.  I will quickly correct anything found to be inaccurate.


For a more complete statement about the author and Pollution Action, please go to www.pollutionaction.org


Don Meulenberg

Pollution Action

Fredericksburg, VA, USA






Appendix A: Studies associating autism with breastfeeding:


A 2011 study that investigated data from all 50 U.S. states and 51 U.S. counties found that "exclusive breast-feeding shows a direct epidemiological relationship to autism," and also, "the longer the duration of exclusive breast-feeding, the greater the correlation with autism." 39



Note that, according to the EPA, Epidemiologic studies of exposed human populations provide the most convincing evidence of human health effects.”43  Also, a dose-response relationship between an exposure and a health outcome is considered to be especially significant evidence to support a finding of cause and effect.  One example of a dose-response relationship, as found in a study by a well-published scientist (R.J. Shamberger), was quoted in the previous paragraph.  This finding was even more significant in that it was based on investigation of a very large, diversely-populated geographic area (all 50 U.S. states), and it also applied in relation to numerous smaller-scale units (51 counties). 


Additional support for a causal connection between breastfeeding and autism was provided by three additional, relatively recent studies, with a dose-response relationship being apparent in the different degrees of correlation with autism according to the different durations of breastfeeding, when these three studies are seen together.

-- In a 2011 Canadian study of a population of over 125,000, using discharge from the hospital as the dividing line for breastfeeding exposure, there was a 25% higher autism rate among the breastfed children than among non-breastfed children.40

-- In a 2009 U.K. study, the duration of breastfeeding that was assessed was four weeks versus less than that, with 65% of the autism cases having received breastfeeding for at least four weeks; that should be compared with only about 28% of the general U.K. infant population (where breastfeeding rates are relatively low) receiving that much breastfeeding; that meant a 130% higher-than-average likelihood of that much breastfeeding history among those with autism. 41

-- In a 2010 American study in Kentucky by two MD’s, the duration of breastfeeding used for comparison was six months, and 37% of autism cases had received that much breastfeeding, compared with 13% of the controls, indicating an approximately 185% (37%/13%) greater likelihood that the autism cases would have had more breastfeeding; the p-value was .003, meaning three chances out of a thousand that the finding was a result of chance occurrence.42



The study described next, in Appendix B below, also shows strong associations between breastfeeding (as a pathway for environmental toxins) and traits of autism.




Appendix B:  Emissions from municipal incinerators were found to be associated with autism-related outcomes far more in children who had been breastfed for six months than in the general population:


Authors of a 2013 study in Taiwan (Lung et al.44) worked with data from over 21,000 children, 953 of whom lived within three kilometers of a municipal incinerator.  The study reported about effects of local incinerators on children, as indicated by parental concerns in specific developmental areas and at certain ages. (They cited other studies as having found parental observations to be valid.)  In children who had been breastfed for at least six months, adverse effects associated with the local incinerator on measured outcomes were reported in all four developmental areas that were asked about, compared with only one area of significant effect on children in the general population with similar exposures to emissions.  Also, the effects (β values) were found to be far greater and the statistical significance far higher (p< .001 in three areas) in breastfed children in all four cases, compared with the data for the one association seen in children in the general population.45


All of the areas in which breastfed children were seen to have worse development were areas that are traits of autism, as follows:   

-- deficits in social development are a core characteristic of ASD,  

-- language impairment is a very common trait of those with ASD, 46 and

-- clumsiness is a common trait of those with ASD; 46 consider this in relation to the study's findings of associations of breastfeeding with adverse effects on both gross motor development and fine motor development, as found at various times of measurement in this study.


When discussing the relationships between incinerator emissions, breastfeeding, and adverse effects on neurological development, the authors said that "children who were breastfed and living within three kilometers of an incinerator were at higher risk of showing mild U/DDD" (emphasis added); and they commented that their findings suggested that "toxins can be transmitted via breastfeeding by mothers who are exposed."  They referred specifically to dioxins, PCBs and mercury as having been found to be significantly present in incinerator emissions, and cited two studies as having reported about dioxins in milk of women living near incinerators.



Appendix C:  Correlation of autism prevalence with exposure to traffic-related toxins also pertains to other states among the cold, northern-most U.S. states:


Consideration of exposure to traffic-related toxins associated with population density also pertains to other states among the northern-most U.S. states -- North Dakota, Montana, Washington, Massachusetts and Maine:

   a) North Dakota has three of the 25 coldest U.S. cities with over 50,000 residents but also has very low overall population density (9 per sq. mile as of year 200066c); so its well-below-average autism rate is in line with expected minimal effects of traffic-related PCB exposures in this state;

 Fig. 1.c

ME_MNsolar.jpg   b) Montana has very low population density (6 per sq. mile in 200066c) and does not have even one of the coldest 50 U.S. cities of over 50,000; so it has neither of those risk factors for high exposures to toxic traffic-related emissions that we have discussed.  And Montana has an autism rate less than half the national average.70  That should be expected, if our concerns about effects of developmental toxins in traffic-related pollution are valid.


Washington is a state with average population density, but its autism rate is not above average despite being another one of the northernmost U.S. states.70  But this is still fully compatible with our hypothesis, since (due to the warming effect of the Pacific Ocean) its northern location does not translate to extremes of cold; it does not have even one of the top 100 coldest U.S. cities with populations over 50,000. 69  


Another of the northernmost U.S states, Maine, has only one cold city with over 50,000 residents, yet it is shown to have the third highest rate of autism in the U.S., far above the national average. (see Figure 1.b)  Clearly there are other factors that affect autism in addition to exposure to nearby-traffic-related pollution and cold weather.  See below.

Fig. 1.d

image008 (2).jpg



Effects of traffic-related pollution can extend well beyond the immediate areas where the toxins are emitted.  PCBs can be carried long distances in air.70b  Maine (extending to the north and east from Portland in the upper-right corner of this weather map) has the misfortune of being downwind from the long, densely-populated, heavily-trafficked Northeast Corridor, which extends from Washington, D.C. area in the mid-east coast up through New York City and on to the Boston area. 

The wind pattern shown in this chart is typical of prevailing wind directions in the northern hemisphere.70a  Emissions from ships going to and from east coast ports, and the associated activities of seaport freight-handling and dredging equipment, would contribute to the general vehicular-traffic-related pollution along this corridor.


The above discussion also relates to Massachusetts (see Boston just to the south from Portland), which is shown by the Department of Education to have an autism rate very slightly higher than that of Maine.(see Figure 1.b above)  Massachusetts is closer than Maine to the direct effects of the drift of emissions up the Northeast Corridor; in addition, Massachusetts has population density ten times the national average, with all that implies about exposures to toxins emitted by local traffic; that should be compared with Maine's density which is half the national average.66c


But Maine definitely has a colder climate and less sun exposure (see Figure 1.c above), which would lead to longer lives of the traffic-related pollutants; this would in turn be linked to effects that could be on the same general scale as the effects of the (greater) exposure to traffic pollution in more-densely populated Massachusetts. 







1)  Kalkbrenner et al., Environmental Chemical Exposures and Autism Spectrum Disorders: A Review of the Epidemiological Evidence, Curr Probl Pediatr Adolesc Health Care, Author manuscript; available

in PMC 2016 May 4, at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4855851/


1a) Project TENDR: Targeting Environmental Neuro-Developmental Risks The TENDR Consensus Statement, Environ Health Perspect. 2016 Jul; 124(7): A118–A122. at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4937840/


1b) P. 96 of EPA:  America's Children and the Environment, at https://www.epa.gov/sites/production/files/2015-06/documents/ace_2003.pdf


1c) Raz et al., Traffic-Related Air Pollution and Autism Spectrum Disorder: A Population-Based Nested Case-Control Study in Israel, American Journal of Epidemiology, Volume 187, Issue 4, 1 April 2018, at https://academic.oup.com/aje/article-abstract/187/4/717/4083712?redirectedFrom=fulltext


2) DellaValle et al., Environmental determinants of polychlorinated biphenyl concentrations in residential carpet dust, Environ Sci Technol. 2013 Sep 17; 47(18): 10405–10414. at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4076890


3) p. 171 of WHO Europe, Special Programme on Health and Environment:  Effects of Air Pollution on Children's Health and Development, 2005, at http://www.ihealthbank.org/Portals/0/Environmental%20Health%20in%20Emergencies/e86575.pdf#page=167


3a)  Laroo et al., Emissions of PCDD/Fs, PCBs, and PAHs from legacy on-road heavy-duty diesel engines, Chemosphere, 2012 Nov at https://www.ncbi.nlm.nih.gov/pubmed/22682896

  Also Hsieh et al., Reduction of Toxic Pollutants Emitted from Heavy-duty Diesel Vehicles by Deploying Diesel Particulate Filters, Aerosol and Air Quality Research, 2011, at http://aaqr.org/VOL11_No6_November2011/8_AAQR-11-05-OA-0058_709-715.pdf


3b) Lehmann et al., Evaluating Health Risks from Inhaled Polychlorinated Biphenyls:  Research Needs for Addressing Uncertainty, Environ Health Perspect/; DOI:10.1289/ehp.1408564 at https://ehp.niehs.nih.gov/1408564/


4) Cortés et al., PCDD/PCDF and dl-PCB in the ambient air of a tropical Andean city:  passive and active sampling measurements near industrial and vehicular pollution sources, Sci Total Environ. <#> 2014 Sep 1 at https://www.ncbi.nlm.nih.gov/pubmed/24555963  Note that PCDD/F is a designation for what is more commonly referred to as dioxins.


4a)  P. 417 of U.S. ATSDR:  Toxicological Profile for Polychlorinated Biphenyls (PCBs), 2000 at http://www.atsdr.cdc.gov/toxprofiles/tp17.pdf  Also p. 411: "PCBs are readily absorbed through the gastrointestinal tract, respiratory system, and skin."   

p. 179 of U.S. ATSDR, Persistent chemicals found in breast milk, Appendix A, at https://www.atsdr.cdc.gov/interactionprofiles/ip-breastmilk/ip03-a.pdf  "...studies of humans and animals exposed to airborne PCBs provide qualitative information that inhaled PCBs can be absorbed (ATSDR 2000). Ingested PCBs appear to be efficiently absorbed based on studies of infants consuming PCBs in their mothers’ breast milk and studies of animals indicating retention percentages ranging from 60 to 100% of ingested doses."

   See also DO Carpenter, Polychlorinated biphenyls and human health, in International Journal of Occupational Medicine and Environmental Health 11(4):291-303, February 1998, p. 4 at https://www.researchgate.net/publication/13261771_Polychlorinated_biphenyls_and_human_health 


4b) Oregon Department of Environmental Quality Environmental Cleanup Program, Oct. 2010, 10-LQ-023, p. D2-4 (attachment 2 of Appendix D, near very end) at http://www.deq.state.or.us/lq/pubs/docs/cu/HumanHealthRiskAssessmentGuidance.pdf 

Quoting, “The doses of PCBs that a breastfeeding infant may be expected to receive, given breast milk PCB concentrations measured in the literature, are presented in table 1. These doses range from 0.0019 to 0.0081 mg/kg/day and are 63-270 times higher than ATSDR’s minimal risk level (0.00003 mg/kg/day) for PCB exposures that last between 15 and 364 days.”


4c) D.O. Carpenter, Polychlorinated Biphenyls (PCBs): Routes of Exposure and Effects on Human Health, in Reviews on environmental health,  21(1):1-23 · January 2006, at https://www.researchgate.net/publication/7081925_Polychlorinated_Biphenyls_PCBs_Routes_of_Exposure_and_Effects_on_Human_Health



4d) p. 569 of U.S. ATSDR:  Toxicological Profile for Polychlorinated Biphenyls (PCBs), 2000 at http://www.atsdr.cdc.gov/toxprofiles/tp17.pdf   "...PCBs tend to accumulate in breast milk fat."


4e)  See Section 2.a of www.pollution-effects.info


5) Section 4.1 of ATDSR document on PBDEs at http://www.atsdr.cdc.gov/toxprofiles/tp68-c4.pdf


6) Re presence of PBDEs in vehicular emissions, citing two other studies as well as its own findings about PBDEs in vehicular emissions, see Lien-Te Hsieh et al., Reduction of Toxic Pollutants Emitted from Heavy-duty Diesel Vehicles by Deploying Diesel Particulate Filters,  Aerosol and Air Quality Research, at http://aaqr.org/VOL11_No6_November2011/8_AAQR-11-05-OA-0058_709-715.pdf ;

    re PBDEs being produced in vehicle emissions in larger amounts than PCBs, see Table 3, Total PCBs and Table 4, Total (PBDEs), ("before" in both cases), noting that PBDEs are shown in nanograms, which must be multiplied by 1000 to be equivalent to the picograms by which the PCBs are quantified.

    also from that study, "The GM PBDE concentrations measured from the exhaust of UGFVs (unleaded gasoline-fueled vehicles) and DFVs (diesel-fueled vehicles) were 46.7 ng/Nm3, and 29.1 ng/Nm3, respectively (Wang et al., 2010b), and the highly brominated PBDEs in urban ambient air were contributed by combustion sources, such as vehicles (Wang et al., 2010b, 2011)."


6.a) See Section 3.b of http://www.pollution-effects.info, which includes many citations of authoritative sources.


7) Johnson-Restrepo et al., An assessment of sources and pathways of human exposure to polybrominated diphenyl ethers in the United States, Chemosphere, 2009 Jul;76(4):542-8. doi: 10.1016/j.chemosphere.2009.02.068. Epub 2009 Apr 5.  at http://www.ncbi.nlm.nih.gov/pubmed/19349061 


8) Grandjean P, Landrigan PJ. Developmental neurotoxicity of industrial chemicals. Lancet. 2006;368:2167–2178. at http://www.reach-compliance.eu/english/documents/studies/neurotoxity/PGrandjean-PjLandrigan.pdfp. 2 

-- Also see see Section 2.b of http://www.pollution-effects.info


9) Gyalpo et al., Insights into PBDE Uptake, Body Burden, and Elimination Gained from  Australian Age–Concentration Trends Observed Shortly after Peak Exposure, Environ Health Perspect 2015 Oct; 123(10): 978–984.at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4590757/


9a) See Section 3 of www.pollution-effects.info.


9b)  See Section 2 of www.pollution-effects.info


9c)  EPA document, Report on the Environment:  Particulate Matter Emissions   http://www.epa.gov/roe/

9d) Pp. 160, 161 of EPA document on Biomonitoring (PBDEs) at https://www.epa.gov/sites/production/files/2015-05/documents/biomonitoring-pbdes.pdf

   See also  Jones-Otazo, Is House Dust the Missing Exposure Pathway for PBDEs? An Analysis of the Urban Fate and Human Exposure to PBDEs, Environ. Sci. Technol. June 15, 2005 at http://pubs.acs.org/doi/abs/10.1021/es048267b


9e)  See Section 2.b of http://www.pollution-effects.info


10) Wang et al., Polybrominated diphenyl ethers in various atmospheric environments of Taiwan: Their levels, source identification and influence of  combustion sources, Chemosphere 2911, Volume 84, Issue 7 at http://www.sciencedirect.com/science/article/pii/S0045653511006515


11) Shi et al., Monitoring of Airborne Polybrominated Diphenyl Ethers in the Urban Area by Means of Road Dust and Camphor Tree Barks, Aerosol and Air Quality Research, 14: 1106–1113, 2014, at http://aaqr.org/VOL14_No4_June2014/3_AAQR-12-11-OA-0304_1106-1113.pdf


12) Re presence of PBDEs in vehicular emissions, citing two other studies as well as its own findings about PBDEs in vehicular emissions, see Lien-Te Hsieh et al., Reduction of Toxic Pollutants Emitted from Heavy-duty Diesel Vehicles by Deploying Diesel Particulate Filters,  Aerosol and Air Quality Research, at http://aaqr.org/VOL11_No6_November2011/8_AAQR-11-05-OA-0058_709-715.pdf ;

    also from that study, "The GM PBDE concentrations measured from the exhaust of UGFVs (unleaded gasoline-fueled vehicles) and DFVs (diesel-fueled vehicles) were 46.7 ng/Nm3, and 29.1 ng/Nm3, respectively (Wang et al., 2010b), and the highly brominated PBDEs in urban ambient air were contributed by combustion sources, such as vehicles (Wang et al., 2010b, 2011)."


13) Johnson-Restrepo et al., An assessment of sources and pathways of human exposure to polybrominated diphenyl ethers in the United States, Chemosphere, 2009 Jul;76(4):542-8. doi: 10.1016/j.chemosphere.2009.02.068. Epub 2009 Apr 5.  at http://www.ncbi.nlm.nih.gov/pubmed/19349061 


14) Gascon et al., Polybrominated Diphenyl Ethers (PBDEs) in Breast Milk and Neuropsychological Development in Infants   US National Library of Medicine National Institutes of Health  Environ Health Perspect  v.120(12); Dec 2012 > PMC3548276   Environ Health Perspect. 2012 December; 120(12): 1760–1765.  at www.ncbi.nlm.nih.gov/pmc/articles/PMC3548276


14a)  Jakobsson et al., Polybrominated diphenyl ethers in maternal serum, umbilical cord serum, colostrum and mature breast milk. Insights from a pilot study and the literature,  Environment International 47 (2012), especially Table 2, at http://www.sciencedirect.com/science/article/pii/S0160412012001183


14b) See Section 3.b of www.pollution-effects.info


14c) Mercury typically 8 parts per billion in breast milk, according to U.S. ATSDR document on mercury at http://www.atsdr.cdc.gov/toxprofiles/tp46-c5.pdf, p. 443,  which compares with1 microgram per liter (1 microgram per billion micrograms), or 1 part per billion, the WHO guideline value for drinking water:  (WHO, Mercury in Drinking-water Background document for development of WHO Guidelines for Drinking-water Quality  WHO/SDE/WSH/03.04/10  at http://www.who.int/water_sanitation_health/dwq/chemicals/en/mercury.pdf  p. 8   Accessed 4/8/2014)

  Also Code of Federal Regulations, Title 21, Chapter 1, Subchapter B, Part 165, Subpart B, Sec. 165-110 at  http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfCFR/CFRSearch.cfm?fr=165.110



15) EPA:  An Alternatives Assessment for the Flame Retardant Decabromodiphenyl Ether (DecaBDE), 2014. at http://www.epa.gov/sites/production/files/2014-05/documents/decabde_final.pdf


17) Gascon et al., Polybrominated Diphenyl Ethers (PBDEs) in Breast Milk and Neuropsychological Development in Infants   US National Library of Medicine National Institutes of Health  Environ Health Perspect  v.120(12); Dec 2012 > PMC3548276   Environ Health Perspect. 2012 December; 120(12): 1760–1765.  at www.ncbi.nlm.nih.gov/pmc/articles/PMC3548276


18) “Food and beverages” row in Table 1 of Health Canada:  Human Health State of the Science Report on Decabromodiphenyl Ether (decaBDE), Dec. 2012,  at https://www.ec.gc.ca/ese-ees/92D49BA9-4B11-4C56-BDB0-9A725C5F688E/DecaBDE%20-%20Final%20SoS%20-%20EN.pdf  Note that, although decaBDE can consist of more than just BDE 209, the two are in practice so similar that the two designations are often used interchangeably. (Costa et al., Is decabromodiphenyl ether (BDE-209) a developmental neurotoxicant?  Neurotoxicology. 2011 Jan)


19) Frederiksen et al., Human internal and external exposure to PBDEs--a review of levels and sources. Int J Hyg Environ Health. 2009 Mar; at https://www.ncbi.nlm.nih.gov/pubmed/18554980


20) 2009 EPA Polybrominated Diphenyl Ethers Action Plan at  http://www.epa.gov/sites/production/files/2015-09/documents/pbdes_ap_2009_1230_final.pdf, p. 12

    Also see Section 2 of www.pollution-effects.info). 


21) 2004 International Emissions Inventory Conference, Air Toxics Session, Clearwater, Florida, Mercury Emissions from Motor Vehicles, at http://www.epa.gov/ttnchie1/conference/ei13/toxics/baldauf_pres.pdf

 Also,  Hoyer et al., Mercury Emissions from Motor Vehicles (EPA publication), esp. p 4, at http://www.epa.gov/ttnchie1/conference/ei13/toxics/hoyer.pdf


22) p.389 of U.S. ATSDR:  Toxicological Profile For Mercury, 1999, at  http://www.atsdr.cdc.gov/toxprofiles/tp46.pdf.

   See also U.S. EPA, Mercury Study, Report to Congress, c7o032-1-1, Volume II:  An Inventory of Anthropogenic Mercury Emissions in the United States, p. 5-7, at http://www.epa.gov/ttn/oarpg/t3/reports/volume2.pdf


23) Table 4 of Singh et al., Quantifying uncertainty in measurement of mercury in suspended particulate matter by cold vapor technique using atomic absorption spectrometry with hydride generator, Springerplus. 2013; 2: 453.  doi:  10.1186/2193-1801-2-453  at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3786082/


23a) ATSDR's Toxic Substances Portal for mercury at



23b) p. 4 and p. 29 of U.S. ATSDR:  Toxicological Profile For Mercury, 1999, at  http://www.atsdr.cdc.gov/toxprofiles/tp46.pdf


23c) p. 379 of  above ATSDR document.


23d)  NIH web page on Polychlorinated Biphenyls at https://ntp.niehs.nih.gov/ntp/roc/content/profiles/polychlorinatedbiphenyls.pdf


24) Chien LC, et al., Analysis of the health risk of exposure to breast milk mercury in infants in Taiwan. Chemosphere. 2006 Jun;64(1):79-85. Epub 2006 Jan 25 at http://www.ncbi.nlm.nih.gov/pubmed/16442149


24a) See Section 3.d of www.pollution-effects.info


25) Newman et al., Traffic-Related Air Pollution Exposure in the First Year of Life and Behavioral Scores at Seven Years of Age, Environ Health Perspect., http://dx.doi.org/10.1289/ehp.1205555 Online 21 May 2013, at http://admin.indiaenvironmentportal.org.in/files/file/Traffic-Related Air Pollution.pdf


25a)  U.S. EPA web page on air pollution trends at https://gispub.epa.gov/air/trendsreport/2016/


26) AAFP:  Breastfeeding, Family Physicians Supporting (Position Paper) -- at http://www.aafp.org/about/policies/all/breastfeeding-support.html


27) Riordan et al., Basics of breastfeeding. Part I: Infant feeding patterns past and present, JOGN Nurs., 1980 Jul-Aug;9(4):207-10, at http://www.ncbi.nlm.nih.gov/pubmed/7001126

Other sources report the low point of breastfeeding to be 1971, based on breastfeeding “ever” or “at any time,” as opposed to the more extended breastfeeding that is more significant regarding health effects.


28) P Grandjean and AA Jensen, Breastfeeding and the Weanling’s Dilemma   Am J Public Health. 2004 July; 94(7): 1075.   PMCID: PMC1448391 at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1448391/ 

-- Also, according to Encyclopedia Britannica, use of insecticides was considered to be responsible for a dramatic increase in agricultural productivity between 1945 and 1965. (https://www.britannica.com/technology/insecticide)


29) Perrin et al., The Increase of Childhood Chronic Conditions in the United States, JAMA, June 27, 2007—Vol 297, No. 24,  2755 at http://www.childrensdayton.org/cms/resource_library/files/a6b01f3b8f8d5ebd/increasedchildhoodchronicjama_07.pdf

30) "Atopic dermatitis,"  Bieber T  N Engl J Med. 2008 Apr 3; 358(14):1483-94.

--  other data found in website of USA Today, posted 8/7/2005, "Allergy sensitivity doubles since 1970s," referring to August 2005 issue of the Journal of Allergy and Clinical Immunology,  found at  http://usatoday30.usatoday.com/news/health/2005-08-07-allergy-sensitivity_x.htm?POE=click-refer


31) see www.breastfeeding-and-asthma.info.  


32) There was no entry for ADHD in the American Psychiatric Association manual until 1968,144 and the first data for ADHD prevalence (for the late 1990’s) showed it to include 6.5% of 5 to 17-year olds. But as of 2011-2013, 14% of U.S. boys age 5 to 17 had been diagnosed with ADHD.147 (CDC data at http://www.cdc.gov/nchs/fastats/adhd.htm) That figure is almost certainly much lower than the percentage in later school years separately, since a fourth of all ADHD cases are not diagnosed until age 9 and later.148


34) Landis et al., Ft. McHenry tunnel study: Source profiles and mercury emissions from diesel and gasoline powered vehicles, Atmospheric Environment, 2007, Volume 41, Issue 38 at http://www.sciencedirect.com/science/article/pii/S1352231007006607


35) Won et al.,  Mercury emissions from automobiles using gasoline, diesel, and LPG, Atmospheric Environment,Volume 41, Issue 35  November 2007, Pages 7547–7552 at http://www.sciencedirect.com/science/article/pii/S1352231007004992


36) Conaway et al., Estimate of mercury emission from gasoline and diesel fuel consumption, San Francisco Bay area, California, Atmospheric Environment 39 (2005)


38) Other studies have been published that are not considered to be relevant here, since they did not take into account major known hazardous components of traffic-related emissions, including PCBs and dioxins;  they assessed only developmental effects of specified other components of traffic pollution. The Volk et al. study, going by distance from the freeways, would have encompassed all components of the vehicular emissions. 

   It has been suggested that particulate-matter pollution (PM) is relevant to traffic-related pollution, but traffic-related pollution is only a minor source of PM among general sources in the environment.  The EPA points out that PM is an indirect result of complex reactions of chemicals from various sources, with automobiles being mentioned as sources only after emissions from power plants and industries; direct emissions of PM from various (non-traffic) sources are also mentioned.  So traffic-related PM could well be15% or less of all PM in air, and only indirectly resulting from traffic at that. 


39) Shamberger, R.J., Autism rates associated with nutrition and the WIC program, J Am Coll Nutr. 2011 Oct;30(5):348-53.  Abstract at www.ncbi.nlm.nih.gov/pubmed/22081621   An image of part of the article is shown below, since it may be expensive for many readers to see the complete study.



40) Dodds et al., The Role of Prenatal, Obstetric and Neonatal Factors in the Development of Autism, J Autism Dev Disord (2011) 41:891–902  DOI 10.1007/s10803-010-1114-8, Table 6, at http://autism.medicine.dal.ca/research/documents/2011DoddsetalJAutDevDisord.pdf   This 2010 Canadian study, drawing data from a population-based clinically-rich perinatal database,” investigated a very large population, nearly 130,000 births.  Data from almost 127,000 of those children (those without identified genetic risk of autism) went into the study’s finding that there was a 25% increased risk of autism among children who were breastfed at discharge from the hospital. 


41) Whitely et al., Trends in Developmental, Behavioral and Somatic Factors by Diagnostic Sub-group in Pervasive Developmental Disorders: A Follow-up Analysis, pp. 10, 14  Autism Insights 2009:1 3-17  at https://www.academia.edu/17814363/Trends_in_Developmental_Behavioral_and_somatic_Factors_by_Diagnostic_sub-group_in_pervasive_Developmental_Disorders_A_Follow-up_Analysis.  This study found that 65% of autism cases had been breastfed for at least four weeks; the authors looked at a comparison figure of 54%, but that figure was unrealistically high, since it came from a study (Pontin et al.) of breastfeeding by mothers largely from “more affluent families”, who breastfeed at unusually high rates in the U.K.   For breastfeeding prevalence data that would apply to the general U.K. population, the authors of the Pontin study referred the reader to Infant Feeding 1995 (Foster et al.); examination of the data in that book reveals that a figure in the upper 20%’s would apply for the equivalent period (just after four weeks). That is also as was found in the U.K. Infant Feeding Survey - UK, 2010 Publication date: November 20, 2012, Chapter 2, at http://www.hscic.gov.uk/catalogue/PUB08694/ifs-uk-2010-chap2-inc-prev-dur.pdf


42)  Breastfeeding and Autism  P. G. Williams, MD, Pediatrics, University of Louisville, and L. L. Sears, MD, presented at International Meeting for Autism Research, May 22, 2010, Philadelphia Marriot  https://imfar.confex.com/imfar/2010/webprogram/Paper6362.html)   This study found a 37% rate of breastfeeding at six months among children diagnosed with autism, as compared with 13% in the control group. 


43) EPA, The Effects of Great Lakes Contaminants on Human Health, Report to Congress, Section III, p. 12 (bottom) and again on p. 16, at http://nepis.epa.gov/Exe/ZyNET.exe/2000BSHI.txt?ZyActionD=ZyDocument&Client=EPA&Index=1995%20Thru%201999&Docs=&Query=&Time=&EndTime=&SearchMethod=1&TocRestrict=n&Toc=&TocEntry=&QField=&QFieldYear=&QFieldMonth=&QFieldDay=&UseQField=&IntQFieldOp=0&ExtQFieldOp=0&XmlQuery=&File=D%3A%5CZYFILES%5CINDEX%20DATA%5C95THRU99%5CTXT%5C00000002%5C2000BSHI.txt&User=ANONYMOUS&Password=anonymous&SortMethod=h%7C-&MaximumDocuments=1&FuzzyDegree=0&ImageQuality=r75g8/r75g8/x150y150g16/i425&Display=p%7Cf&DefSeekPage=x&SearchBack=ZyActionL&Back=ZyActionS&BackDesc=Results%20page&MaximumPages=10&ZyEntry=20


44) Lung et al., Incinerator Pollution and Child Development in the Taiwan Birth Cohort Study,  Int. J. Environ. Res. Public Health 2013, especially the Supplemental Materials, at www.mdpi.com/1660-4601/10/6/2241/pdf


45) As stated in the Supplemental Material of the Lung et al. study above, the adverse associations in breastfed children were found with p values of 0.003, 0.011, and 0.001 (four at 0.001); all of these were much lower (less likely to result from chance) than the p value of .017 for the one area in which there was significant effect of local incineration on children in the general population.


46)  See list of symptoms of ASD at http://www.autismkey.com/autism-symptoms/


47) Suglia et al., Association of Black Carbon with Cognition among Children in a Prospective Birth Cohort Study, at American Journal of Epidemiology, Vol. 167, Issue 3, February 2008 at https://www.ncbi.nlm.nih.gov/pubmed/18006900


48) Sunyer et al., Association between Traffic-Related Air Pollution in Schools and Cognitive Development in Primary School Children: A Prospective Cohort Study, PLOS, March3, 2015, http://dx.doi.org/10.1371/journal.pmed.1001792


49) Harris et al., Prenatal and Childhood Traffic-Related Pollution Exposure and Childhood Cognition in the Project Viva Cohort (Massachusetts, USA),  Environ Health Perspect. 2015 October; 123(10): 1072–1078.  Published online 2015 April 3. doi:  10.1289/ehp.1408803 PMCID: PMC4590752, at http://pubmedcentralcanada.ca/pmcc/articles/PMC4590752/

50) Min et al., Exposure to ambient PM10 and NO2 and the incidence of attention-deficit hyperactivity disorder in childhood, Environment International, Vol. 99, Feb 2017, at http://www.sciencedirect.com/science/article/pii/S0160412016308881


51) Clifford et al., Exposure to air pollution and cognitive functioning across the life course – A systematic literature review, Environmental Research, 147 (2016)


52) Brockmeyer et al., How air pollution alters brain development: the role of neuroinflammation, DeGruyter Open, 2016, at https://www.degruyter.com/downloadpdf/j/tnsci.2016.7.issue-1/tnsci-2016-0005/tnsci-2016-0005.xml


53) Kalkbrenner et al, Particulate Matter Exposure, Prenatal and Postnatal Windows of Susceptibility, and Autism Spectrum Disorders, Epidemiology • Volume 26, Number 1, January 2015  at https://www.researchgate.net/publication/266626245_Particulate_Matter_Exposure_Prenatal_and_Postnatal_Windows_of_Susceptibility_and_Autism_Spectrum_Disorders


53a) Waldman et al., Autism Prevalence and Precipitation Rates in

California, Oregon, and Washington Counties, Arch Pediatr Adolesc Med/Vol 162 (No. 11), Nov 2008


53b)  See www.pesticides-and-breastfeeding.info.


53c)  p. 530 of U.S. ATSDR:  Toxicological Profile for Polychlorinated Biphenyls (PCBs), 2000 at http://www.atsdr.cdc.gov/toxprofiles/tp17.pdf

    Ospar Commission, Monitoring and Assessment Series, Atmospheric deposition of selected heavy metals and persistent organic pollutants to the OSPAR Maritime Area (1990 - 2005), at http://qsr2010.ospar.org/media/assessments/p00375_Atmospheric_deposition_HM_and_POPs.pdf


53d) U.S. ATSDR:  Toxicological Profile for Mercury, 1999, at  http://www.atsdr.cdc.gov/toxprofiles/tp46.pdf


53e) U.S. EPA web page on bioaccumulation at https://www.epa.gov/sites/production/files/documents/bioaccumulationbiomagnificationeffects.pdf

  Also EPA web page on PBDEs at https://www.epa.gov/assessing-and-managing-chemicals-under-tsca/polybrominated-diphenyl-ethers-pbdes


53f) Milbrath et al.,Apparent Half-Lives of Dioxins,Furans, and Polychlorinated Biphenyls as a Function of Age, Body Fat, Smoking Status, and Breast-Feeding. Environ Health Perspect 117:417–42 at https://ehp.niehs.nih.gov/11781/


53g) CDC Biomonitoring Summary of PBDEs at https://www.cdc.gov/biomonitoring/PBDEs_BiomonitoringSummary.html


53h) U.S. ATSDR, Persistent chemicals found in breast milk,  Appendix A, p. 180, at https://www.atsdr.cdc.gov/interactionprofiles/ip-breastmilk/ip03-a.pdf


53j)  p. 178 of National Academies Press, Hormonally Active Agents in the Environment (1999), Chapter: 6:  Neurologic Effects, at http://www.nap.edu/read/6029/chapter/8#178


53k) See Section B above and also Sections 2.a, 2.b and 2.d of www.pollution-effects.info for detailed discussions of this topic, including references to authoritative sources.


53m)  Univ. of Minnesota document on mercury at http://enhs.umn.edu/current/5103_spring2003/mercury/mercdose.html


54) CDC of breastfeeding data by states for 2010  at https://www.cdc.gov/breastfeeding/data/nis_data/rates-any-exclusive-bf-state-2010.htm


55) Talbott et al., Fine particulate matter and the risk of autism spectrum disorder, Environmental Research 40 (2015) at https://www.researchgate.net/profile/Jane_Clougherty/publication/276147082_Fine_particulate_matter_and_the_risk_of_autism_spectrum_disorder/links/55d38cbc08ae0a3417226a63/Fine-particulate-matter-and-the-risk-of-autism-spectrum-disorder.pdf


56) See Sections 2 and 9 of www.pollution-effects.info


57) See Section 3.f of http://www.pollution-effects.info


58) Sexton et al. 1993. Air pollution health risks: do class and race matter? Toxicol Ind Health 9(5):843–878).

   Krieger et al., Black carbon exposure, socioeconomic and racial/ethnic spatial polarization, and the Index of Concentration at the Extremes (ICE), Health and Place, Vol. 34, July 2015, at http://www.sciencedirect.com/science/article/pii/S135382921500074X

 . Tian et al., Evaluating socioeconomic and racial differences in traffic-related metrics in the United States using a GIS approach, Journal of Exposure Science and Environmental Epidemiology 23, 215-222 (March/April 2013) | doi:10.1038/jes.2012.83 at http://www.nature.com/jes/journal/v23/n2/full/jes201283a.html


59)  See CDC data on breastfeeding rates by socio-demographics at https://www.cdc.gov/breastfeeding/data/nis_data/rates-any-exclusive-bf-socio-dem-2010.htm


59b) Jessri et al., Predictors of exclusive breastfeeding: observations from the Alberta pregnancy outcomes and nutrition (APrON) study, BMC Pediatrics 2013*13*:77, at http://bmcpediatr.biomedcentral.com/articles/10.1186/1471-2431-13-77  


60)  Mocarelli et al., Perinatal Exposure to Low Doses of Dioxin Can Permanently Impair Human Semen Quality, Environ Health Perspect. May 2011; 119(5): 713–718. Published online Jan 24, 2011. doi:  10.1289/ehp.1002134  at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3094426/


61)  U.S. ATSDR:  Toxicological Profile for Polychlorinated Biphenyls (PCBs), 2000 at http://www.atsdr.cdc.gov/toxprofiles/tp17.pdf, p. 569


62)  Drexler et al., The mercury concentration in breast milk resulting from amalgam fillings and dietary habits,  Environ Res. 1998 May;77(2):124-9. at   http://www.ncbi.nlm.nih.gov/pubmed/9600805.  


63)  Vahter et al., Longitudinal Study of Methylmercury and Inorganic Mercury in Blood and Urine of Pregnant and Lactating Women, as Well as in Umbilical Cord Blood, Environmental Research, Section A 84, 186}194 (2000) at http://www.detoxmetals.com/content/FISH/FISH/Hg%20in%20pregnant%20urine%20and%20cord.pdf


64)  Infant Exposure to Dioxin-like Compounds in Breast Milk  Lorber and Phillips  Vol. 110 | No. 6 | June 2002 • Environmental Health Perspectives http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=54708#Download


65)  Regarding link between autism and vitamin D deficiency, see also Fernell et al., Autism spectrum disorder and low vitamin D at birth: a sibling control study,  Molecular Autism,  January 2015, at http://molecularautism.biomedcentral.com/articles/10.1186/2040-2392-6-3


66)  Wong et al., Degradation of Polychlorinated Biphenyls by UV-Catalyzed Photolysis, Human and Ecological Risk Assessment: An International Journal, Volume 12, 2006 - Issue 2 at http://www.tandfonline.com/doi/abs/10.1080/10807030500531547?queryID=%24%7BresultBean.queryID%7D&


66a) Decomposition of PBDEs by Direct Photolysis in Marine Surface Waters,  January 2007  Kuivikko et al.,  Laboratory of Analytical Chemistry, Department of Chemistry, University of Helsinki, Finland), at https://www.researchgate.net/publication/242592465_Decomposition_of_PBDEs_by_Direct_Photolysis_in_Marine_Surface_Waters


66b) Environmental Science & Technology Online News, 1/18/2007, Dioxins and PCBs in rural areas, at http://www.ldeo.columbia.edu/edu/eesj/gradpubs/sciencemag/NL_ES&TDioxinsandPCBsrural_0107.pdf


66c) U.S. Census Bureau, at https://www.census.gov/2010census/data/apportionment-dens-text.php


66d) Wang et al., Emission estimation and congener-specific characterization of polybrominated diphenyl ethers from various stationary and mobile sources, Environmental Pollution, Vol. 158, Issue 10, Oct. 2010, at http://www.sciencedirect.com/science/article/pii/S0269749110002769


66e) pp. 107 and 111 of Tu et al., Distribution of Polybrominated Dibenzo-p-dioxins and Dibenzofurans and Polybrominated Diphenyl Ethers in a Coal-fired Power Plant and Two Municipal Solid Waste Incinerators, Aerosol and Air Quality Research, 11: 596–615, 2011, doi: 10.4209/aaqr.2011.05.0071 at http://aaqr.org/VOL11_No5_October2011/14_AAQR-11-05-OA-0071_596-615.pdf;

   also, the emissions rate per hour was found to be 14 to 18 times as high for the power plant as for the municipal incinerators


66f) McDonald, Polybrominated diphenylether levels among united states residents:  Daily intake and risk of harm to the developing brain and reproductive organs, Integrated Environmental Assessment and Management, Volume 1, Issue 4, November 2005 at http://onlinelibrary.wiley.com/doi/10.1002/ieam.5630010404/full


66g)  State of Oregon web page on PBDEs at http://public.health.oregon.gov/HealthyEnvironments/HealthyNeighborhoods/ToxicSubstances/Pages/pbde.aspx


66h) Štěpánková et al., Dioxin-Like and Endocrine Disruptive Activity of Traffic-Contaminated Soil Samples,  Arch Environ Contam Toxicol (2009),  at https://www.researchgate.net/publication/26259547_Dioxin-Like_and_Endocrine_Disruptive_Activity_of_Traffic-Contaminated_Soil_Samples;  specifically, Table 3, 1st column re dioxins.


67) Biterna et al., Polychlorinated in ambient air of NW Greece and in particulate emissions, in Environment International, August 2005 at https://www.researchgate.net/publication/7830615_Polychlorinated_in_ambient_air_of_NW_Greece_and_in_particulate_emissions_Environment_International_31_671-677


67a) Table 8.6 of European Environment Agency,  EMEP/CORINAIR Guidebook, Sources of PCB Emissions, 2005


67b) p. 38 of P.H. Dyke, U.K. Environment Agency:  PCB and PAH Releases from Incineration and Power Generation Processes, R&D Technical Report P4-052,  at



67c) Shin et al., Concentration and congener patterns of polychlorinated biphenyls in industrial and municipal waste incinerator flue gas..., 2006, at https://www.researchgate.net/publication/7443263_Concentration_and_congener_patterns_of_polychlorinated_biphenyls_in_industrial_and_municipal_waste_incinerator_flue_gas_Korea


Also, Table 3 of Dyke report in reference 67b above.  16 different sources of emissions of one of the two major types of PCBs (mostly combustion sources) were investigated, and municipal waste incineration was a greater source of this major type of PCBs than the total of all 15 of the other sources combined.


68) Ishaq et al., PCBs, PCNs, PCDD/Fs, PAHs and Cl-PAHs in air and water particulate  samples--patterns and variations, in Chemosphere  March 2003 at https://www.researchgate.net/publication/10934371_PCBs_PCNs_PCDDFs_PAHs_and_Cl-PAHs_in_air_and_water_particulate_samples--patterns_and_variations

   Their highest readings for PCBs (and other toxins) were at locations of unusually high vehicular emissions (road tunnels), and there were decreases in PCB concentrations with increasing distance outbound from concentrated traffic emissions.


69) data provided by City-data.com 2/2017 at http://www.city-data.com/top2/c456.html




70) U.S. Dept of Education, IDEA Section 618 Data Products, choosing item 8, at https://www2.ed.gov/programs/osepidea/618-data/state-level-data-files/index.html#bcc



70a) Infoplease at http://www.infoplease.com/encyclopedia/weather/wind-prevailing-winds-general-circulation-patterns.html


70b)  ATSDR Toxic Substances Portal for PCBs at https://www.atsdr.cdc.gov/toxfaqs/tf.asp?id=140&tid=26


71)  p. 3 of US Geological Survey:  Mercury in Precipitation in Indiana, January 2004–December 2005 , at https://pubs.usgs.gov/sir/2008/5148/pdf/sir2008-5148_web.pdf




Won et al.,  Mercury emissions from automobiles using gasoline, diesel, and LPG, Atmospheric Environment,Volume 41, Issue 35  November 2007, Pages 7547–7552 at http://www.sciencedirect.com/science/article/pii/S1352231007004992


Lorber M, Exposure of Americans to polybrominated diphenyl ethers, J Expo Sci Environ Epidemiol. 2008 Jan;18(1):2-19. Epub 2007 Apr 11. at https://www.ncbi.nlm.nih.gov/pubmed/17426733