Elsevier

Health & Place

Volume 15, Issue 1, March 2009, Pages 18-24
Health & Place

Proximity to point sources of environmental mercury release as a predictor of autism prevalence

https://doi.org/10.1016/j.healthplace.2008.02.001Get rights and content

Abstract

The objective of this study was to determine if proximity to sources of mercury pollution in 1998 were related to autism prevalence in 2002. Autism count data from the Texas Educational Agency and environmental mercury release data from the Environmental Protection Agency were used. We found that for every 1000 pounds of industrial release, there was a corresponding 2.6% increase in autism rates (p<.05) and a 3.7% increase associated with power plant emissions(P<.05). Distances to these sources were independent predictors after adjustment for relevant covariates. For every 10 miles from industrial or power plant sources, there was an associated decreased autism Incident Risk of 2.0% and 1.4%, respectively (p<.05). While design limitations preclude interpretation of individual risk, further investigations of environmental risks to child development issues are warranted.

Introduction

Mercury is a heavy metal found naturally in trace amounts in the earth's atmosphere in differing forms—as elemental vapor, reactive gaseous compounds, or particulate matter. Studies show that background levels of environmental mercury deposition have steadily increased several fold since the pre-industrial era (Schuster et al., 2002), with the largest source of potentially adverse exposures coming primarily from coal-fired utility plants (33%), municipal/medical waste incinerators (29%) and commercial/industrial boilers (18%)—estimated to be responsible for 158 tons of environmental mercury released per year in the US (Environmental Protection Agency, Report to Congress, 1997). Other sources include hazardous waste sites, cement factories, and chlorine production plants. According to the Agency for Toxic Substances and Disease Registry (ATSDR), next to arsenic and lead, mercury is the third most frequently found toxic substance in waste facilities in the United States (ATSDR, 2001).

Mercury is now widespread in the environment (EPA, 1997; ATSDR, 2001). The long-range atmospheric transport of mercury (Ebinghaus et al., 2001), and its conversion to organic forms through bio-accumulation in the aquatic food chain has been known for some time (MacGregor, 1975; Mahaffey, 1999). Notwithstanding, there are emerging concerns over the potential adverse effects of ambient levels of environmental mercury during early childhood development. There is sufficient evidence that children and other developing organisms are particularly susceptible to the adverse neurological effects of mercury (Landrigan and Garg, 2002; Grandjean et al., 1995; Ramirez et al., 2003; Rice and Barone, 2000).

Evidence from animal studies suggests that neonates lack the ability to efficiently excrete both methylmercury (Rowland et al., 1983) and inorganic mercury (Thomas and Smith, 1979), and that there is a higher lactational transfer of inorganic mercury than methylmercury (Sundberg et al., 1991a, Sundberg et al., 1991b). Correspondingly, it has been shown that infants exposed via milk from mothers who were accidentally poisoned by methylmercury-contaminated bread in Iraq accumulated higher mercury concentrations in their blood than did their mothers (Amin-Zaki et al., 1988) and the Faroe Island studies show that hair mercury concentrations in infants increased with the duration of the nursing period (Grandjean et al., 1994). It has also been shown that maternal dental amalgams have been linked to higher body burdens in infants (Oskarsson et al., 1996).

A 10-year longitudinal cohort monitoring study in Finland demonstrated that median hair total mercury concentrations increased in individuals who lived 2 km from a mercury polluting power plant compared to unexposed reference groups living further away (Kurttio et al., 1998). A study performed in China demonstrated that higher mercury concentrations are present in soil sediments and rice fields that are in close proximity to mercury emitting industrial plants and mining operations compared to areas that are more distant (Wang et al., 2003). A variety of similar investigations involving human, plant, and animal studies performed in different global locations consistently demonstrate that mercury concentrations are inversely associated with distance to the environmental source (Ordonez et al., 2003; Fernandez et al., 2000; Hardaway et al., 2002; Navarro et al., 1993; Kalac et al., 1991; Moore and Sutherland, 1981).

A 2000 report by the National Academy of Sciences’ National Research Council estimates that approximately 60,000 children per year may be born in the US with neurological problems due to in utero exposure to methylmercury (NAS, 2000). The neurotoxicity of low-level mercury exposure has only recently been documented (NAS, 2000; EPA, 1997) and little is known about persistent low-dose ambient exposures coming from environmental sources or its influence on childhood developmental disorders such as autism—a condition affecting impairments in social, communicative, and behavior development typically present before age 3 years manifested by abnormalities in cognitive functioning, learning, attention, and sensory processing (Yeargin-Allsopp et al., 2003; CDC, 2007).

One hypothesis, which has been advanced to explain the recently observed increases in autism in the US and Europe, is that biological damage from neurotoxic substances such as mercury may play a causal role (Bernard et al., 2002). Holmes et al. (2003) found that mercury levels in the hair of autistic children were significantly lower than non-autistic controls indicating, according to the authors, that autistic children retain mercury in their body due to impairments in detoxification pathways. After the administration of a heavy metal chelating agent, Bradstreet et al. (2003) demonstrated that autistic children, relative to controls excreted more mercury in urine than non-autistic controls. Two recent studies have shown that body burden of mercury, as indicated by increased levels of urinary porphyrins specific to mercury exposure, are significantly higher in autistic children than in non-autistic children (Nataf et al., 2006; Geier and Geier, 2006).

While the association between autism and thimerisol (a mercury-based preservative formerly used in the childhood vaccination schedule during the 1990s) has not been scientifically established (Freed et al., 2002; Schechter and Grether, 2008), two studies have demonstrated an association with environmental sources of mercury and autism. Windham et al. (2006) demonstrated that ambient air mercury was associated with elevated autism risk in a case–control study in California, and Palmer et al. (2006) demonstrated that environmental mercury pollution was associated with point prevalence estimates of autism using EPA reported mercury release data from 254 counties in Texas. A major limitation to this study was that the cross-sectional design precluded any causal inferences. In addition, exposure was inferred from total pounds of environmentally released mercury aggregated at the county level at a specific point in time. Using distance to potential exposure sources may be a more reasonable proxy for exposure than one defined by total amount contained within artificial county boundaries. Given the literature on the relevance of proximity to the source of mercury and body burden, we suspect that distance to the source of mercury exposure may actually explain, at least in part, the association between increased autism rates and environmental mercury pollution found in both the Palmer et al. (2006) and Windham et al. (2006) studies.

The objective of the current study is to determine if proximity to major sources of mercury pollution is related to autism prevalence rates.

Section snippets

Data source and sample

Data for environmentally released mercury were obtained from the United State Environmental Protection Agency Toxics Release Inventory (TRI) (USEPA-TRI, 2006). TRI collects information about chemical releases and waste management reported by major industrial facilities in the US. The TRI database was established by Section 313 of the Emergency Planning and Community Right-To-Know Act of 1986 (EPCRA). Under EPCRA, industrial facilities in specific sectors are required to report their

Results

Table 1 shows the descriptive statistics of the study variables. Note that there is considerable variation in each variable. Table 2 shows the Poisson regression coefficients and the corresponding Incident Risk Ratio (IRR) for the models exploring the linear and non-linear association between 1998 mercury release from industrial sources, distance, and 2002 autism rates. Model 1a shows that environmentally released mercury in 1998 is significantly associated with autism rates in 2002. We

Discussion

These results build upon two prior studies demonstrating an association between environmental mercury release and autism rates (Palmer et al., 2006; Windham et al., 2006). The current study shows that environmental mercury in 1998 is associated with autism rates in 2002 after adjusting for other relevant sociodemographic covariates including autism rates in 1997. This is consistent with the prior reports. The novel findings in this study are that distance to the sources of mercury release was

References (52)

  • D.J. Thomas et al.

    Distribution and excretion of mercuric chloride in neonatal rats

    Toxicology and Applied Pharmacology

    (1979)
  • D. Wang et al.

    Accumulation and transformation of atmospheric mercury in soil

    Science of the Total Environment

    (2003)
  • L. Amin-Zaki et al.

    Studies of infants postnatally exposed to methylmercury

    Journal of Pediatrics

    (1988)
  • Agency for Toxic Substances and Disease Registry (ATSDR), 2001. CERCLA Priority List of Hazardous Substances. US...
  • S. Bernard et al.

    The role of mercury in the pathogenesis of autism

    Molecular Psychiatry

    (2002)
  • J. Bradstreet et al.

    A case–control study of mercury burden in children with autistic spectrum disorders

    Journal of American Physicians and Surgeons

    (2003)
  • Centers for Disease Control and Prevention, 2007. Prevalence of Autism Spectrum Disorders—Autism and Developmental...
  • R. Ebinghaus et al.

    Measurements of atmospheric mercury with high time resolution: recent applications in environmental research and monitoring

    Fresenius Journal of Analytical Chemistry

    (2001)
  • HA. El-Fawal et al.

    Neuroimmunotoxicology: humoral assessment of neurotoxicity and autoimmune mechanisms

    Environmental Health Perspectives

    (1999)
  • Environmental Protection Agency, 1997. Mercury study report to Congress. Publication number: EPA...
  • G.L. Freed et al.

    The process of public policy formulation: the case of thimerosal in vaccines

    Pediatrics

    (2002)
  • D. Geier et al.

    Prospective Assessment of porphyrins in Autistic disorders: a potential marker for heavy metal exposure

    Neurotoxicity Research

    (2006)
  • P. Grandjean et al.

    Human milk as a source of methylmercury exposure in infants

    Environmental Health Perspectives

    (1994)
  • P. Grandjean et al.

    Milestone development in infants exposed to methylmercury from human milk

    Neurotoxicology

    (1995)
  • C. Hardaway et al.

    Atomic absorption spectrometric determination of chromium, copper, lead, mercury, and zinc in sediments collected in Bayou d’Inde, southwestern Louisiana

    Journal of AOAC International

    (2002)
  • A. Hill et al.

    Stability and interpersonal agreement of the interview-based diagnosis of autism

    Psychopathology

    (2001)
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