Air Pollution and Sudden Infant Death Syndrome (SIDS):
A Selected Annotated Bibliography

This bibliography provides information about the relationship between outdoor and indoor air pollution (with the exception of smoking) and SIDS. Also see the Resource Center bibliography on smoking.

These articles have been selected by Resource Center staff from PubMed, a service of the National Library of Medicine that includes over 19 million citations from MEDLINE and other life science journals for biomedical articles back to 1948. PubMed includes links to full text articles and other related resources.

Availability of full-text journal articles is often limited to subscribers or through inter-library loan. Please see your local library for copies of these articles, or view PubMed's How to Get the Journal Article or Partners in Information Access for the Public Health Workforce's How to Access Journal Articles for more details.

---

Woodruff TJ, Darrow LA, Parker JD.
Air pollution and postneonatal infant mortality in the United States, 1999-2002.
Environ Health Perspect. 2008 Jan;116(1):110-5.

OBJECTIVE: Our goal was to evaluate the relationship between cause-specific postneonatal infant mortality and chronic early-life exposure to particulate matter and gaseous air pollutants across the United States. METHODS: We linked county-specific monitoring data for particles with aerodiameter of < or = 2.5 microm (PM2.5) and < or = 10 microm (PM10), ozone, sulfur dioxide, and carbon monoxide to birth and death records for infants born from 1999 to 2002 in U.S. counties with > 250,000 residents. For each infant, we calculated the average concentration of each pollutant over the first 2 months of life. We used logistic generalized estimating equations to estimate odds ratios of postneonatal mortality for all causes, respiratory causes, sudden infant death syndrome (SIDS), and all other causes for each pollutant, controlling for individual maternal factors (race, marital status, education, age, and primiparity), percentage of county population below poverty, region, birth month, birth year, and other pollutants. This analysis includes about 3.5 million births, with 6,639 postneonatal infant deaths. RESULTS: After adjustment for demographic and other factors and for other pollutants, we found adjusted odds ratios of 1.16 [95% confidence interval (CI), 1.06-1.27] for a 10-mug/m3 increase in PM10 for respiratory causes and 1.20 (95% CI, 1.09-1.32) for a 10-ppb increase in ozone and deaths from SIDS. We did not find relationships with other pollutants and for other causes of death (control category). CONCLUSIONS: This study supports particulate matter air pollution being a risk factor for respiratory-related postneonatal mortality and suggests that ozone may be associated with SIDS in the United States.

 

Omalu BI, Lindner JL, Janssen JK, Nnebe-Agumadu U, Weedn V.
The role of environmental factors in the causation of sudden death in infants: two cases of sudden unexpected death in two unrelated infants who were cared for by the same babysitter.
J Forensic Sci. 2007 Nov;52(6):1355-8. Epub 2007 Sep 15.

We report two cases of sudden unexpected death in two unrelated African American female infants, 2 months and 4 months old. Both infants were attended to by the same babysitter in the same apartment and died 39 days apart in the same bed and in the same bedroom. The autopsy of the first infant revealed sudden unexplained death in an infant. Toxicologic analysis for carbon monoxide (CO) was not performed because it was not suspected. When the second infant died, investigation into the ambient air quality within the apartment revealed high levels of CO emanating from a poorly ventilated and defective hot water heater, which was located across a hallway from the bedroom where the two babies died. CO saturation levels in the postmortem blood samples of the two babies were elevated and were similar (13% and 14%). Nicotine and cotinine were not detected in the blood sample of the two infants. Cherry-red livor mortis was absent. Acute CO intoxication was determined to be the underlying cause of these two unexpected deaths. These two cases underscore the need to integrate ambient air analysis and postmortem CO analysis as routine components of the comprehensive death investigation of infants who die suddenly and unexpectedly.

 

Loghmanee DA, Weese-Mayer DE.
Sudden infant death syndrome: another year of new hope but no cure.
Curr Opin Pulm Med. 2007 Nov;13(6):497-504.

PURPOSE OF REVIEW: Sudden infant death syndrome has inspired increasingly sophisticated studies at a time when rates are declining because of the Back-to-Sleep campaign, but ethnic disparities are widening. This review evaluates and discusses original, recent research in this area. RECENT FINDINGS: The epidemiology of sudden infant death syndrome was evaluated, corroborating known risk factors and identifying new risk factors such as socioeconomic depression and air pollution. Deficits in our understanding of risk factors for this syndrome persist, suggesting a need for ethnicity-specific education, especially among the underserved. Both autopsy and genetic testing were found to improve diagnostic accuracy or identify other causes of death (e.g. long Q-T syndrome). Debate persists over counseling regarding pacifiers and co-sleeping within the context of breastfeeding. Support was found for a relationship between sudden infant death syndrome and autonomic dysregulation via the serotonergic pathway, but more research is needed. SUMMARY: The cause of sudden infant death syndrome remains elusive. Recent studies, however, suggest that improved culturally sensitive educational programs, increased diagnostic specificity, and further clarification of the link between genetics and developmental stage might further decrease the number of infants lost to this devastating disease and elucidate the mechanism(s) responsible for this syndrome.

 

Etzel RA.
Indoor and outdoor air pollution: tobacco smoke, moulds and diseases in infants and children.
Int J Hyg Environ Health. 2007 Oct;210(5):611-6. Epub 2007 Sep 14.

Although outdoor air pollution first brought the issue of air pollution health effects to public attention, it is now indoor air pollution that likely has the greatest impact on children's health. The World Health Organization estimates that the global burden of disease from indoor air pollution is far greater than the burden from outdoor air pollution. This review focuses on two indoor pollutants, one that has been well studied, and another that deserves additional study. There is very strong evidence about the harmful effects of tobacco. Policy to decrease children's tobacco exposure and use should be implemented without delay. The emerging findings linking household inhalation of mould spores and infant pulmonary hemorrhage merit follow-up in other countries, because they may provide clues to some deaths from the sudden infant death syndrome.

 

Heinrich J, Slama R.
Fine particles, a major threat to children.
Int J Hyg Environ Health. 2007 Oct;210(5):617-22. Epub 2007 Sep 4.

BACKGROUND: There is a growing body of evidence for serious health consequences of exposure to ambient air pollution. The general question of who is susceptible is one of the most important gaps in current knowledge regarding particulate matter (PM)-related health effects. Who is susceptible depends on the specific health endpoint being evaluated and the level and length of exposure. Here, we restrict the review on the impact of fine particle exposure on children's health to the following outcomes: infant death, lung function, respiratory symptoms and reproductive outcomes. METHODS: This is a strategic review of children's susceptibility to ambient fine particles and characteristics of infant and children which underlie their increased susceptibility to PM. RESULTS: Ambient fine PM is associated with intra-uterine growth retardation, infant mortality; it is associated with impaired lung function and increased respiratory symptoms, particularly in asthmatics. Concerning infant mortality, exposure to PM is strongly and consistently associated with postneonatal respiratory mortality and less consistently with sudden infant death syndrome. Although most of the studies reported adverse effects for this health outcome, the evidence is weaker than for infant death. Exposure to fine PM has been associated with impaired lung function and lung function growth. Most of the studies reported increased prevalence of symptom with increased exposure to fine PM. CONCLUSION: Fine PM is a major threat to children, because of their higher exposure to PM compared to adults, the immature state of the lung in childhood and also of the immune function at birth. The first months of life might be a period of particular sensitivity. Although the mechanisms of air pollution effects have not yet been completely understood, pregnant women, infants and children need specific protection against exposure to fine particles.

 

Koranteng S, Vargas AR, Buka I.
Ambient air pollution and children's health: A systematic review of Canadian epidemiological studies.

Paediatr Child Health. 2007 Mar;12(3):225-33.

BACKGROUND: There is growing concern about the health effects of ambient air pollution (AP) in children. The present article summarizes and compares local information regarding the adverse effects of AP on the health of Canadian children with reports from elsewhere. METHODS: PUBMED, MEDLINE and EMBASE databases were searched for epidemiological studies, published between January 1989 and December 2004, on the adverse health effects of criteria air pollutants among Canadian children. RESULTS: Eleven studies investigated the association between AP and various respiratory health outcomes, while one study assessed the effect of AP on sudden infant death syndrome. Another study examined the effects of AP on pregnancy outcomes. Most of the available information was from Ontario and British Columbia. Despite inconsistencies among study results and data from elsewhere, evidence from Canadian studies suggest that AP may cause adverse respiratory health effects in children and adverse pregnancy outcomes, and may contribute to infant mortality in Canada. INTERPRETATION: AP has detrimental health effects among Canadian children. Paediatricians and other health care workers with an interest in child health should encourage parents and children to adhere to smog (AP) advisories. Existing regulatory practices should be reviewed to reduce current levels of ambient air pollutants in Canada.

 

Hajat S, Armstrong B, Wilkinson P, Busby A, Dolk H.
Outdoor air pollution and infant mortality: analysis of daily time-series data in 10 English cities.
J Epidemiol Community Health. 2007 Aug; 61(8):719-22.

BACKGROUND: There is growing concern that moderate levels of outdoor air pollution may be associated with infant mortality, representing substantial loss of life-years. To date, there has been no investigation of the effects of outdoor pollution on infant mortality in the UK. METHODS: Daily time-series data of air pollution and all infant deaths between 1990 and 2000 in 10 major cities of England: Birmingham, Bristol, Leeds, Liverpool, London, Manchester, Middlesbrough, Newcastle, Nottingham and Sheffield, were analysed. City-specific estimates were pooled across cities in a fixed-effects meta-regression to provide a mean estimate. RESULTS: Few associations were observed between infant deaths and most pollutants studied. The exception was sulphur dioxide (SO2), of which a 10 mug/m(3) increase was associated with a RR of 1.02 (95% CI 1.01 to 1.04) in all infant deaths. The effect was present in both neonatal and postneonatal deaths. CONCLUSIONS: Continuing reductions in SO2 levels in the UK may yield additional health benefits for infants.

 

Anderson ME, Bogdan GM.
Environments, indoor air quality, and children.
Pediatr Clin North Am. 2007 Apr;54(2):295-307.

This article addresses air-quality science in the indoor environments in which children and adolescents find themselves, including the home, the school, and other environments such as work and recreational situations. The home arena is covered extensively, presenting an analysis of the usual exposures such as environmental tobacco smoke and bioaerosols and also touching on discrete issues such as sudden infant death syndrome, carbon monoxide, and public housing. Recreation and work environments are covered as well.

 

Ritz B, Wilhelm M, Zhao Y.
Air pollution and infant death in southern California, 1989-2000.
Pediatrics. 2006 Aug; 118(2):493-502.

Objective: We evaluated the influence of outdoor air pollution on infant death in the South Coast Air Basin of California, an area characterized by some of the worst air quality in the United States. Methods: Linking birth and death certificates for infants who died between 1989 and 2000, we identified all infant deaths, matched 10 living control subjects to each case subject, and assigned the nearest air monitoring station to each birth address. For all subjects, we calculated average carbon monoxide, nitrogen dioxide, ozone, and particulate matter < 10 microm in aerodynamic diameter exposures experienced during the 2-week, 1-month, 2-month, and 6-month periods before a case subject's death. Results: The risk of respiratory death increased from 20% to 36% per 1-ppm increase in average carbon monoxide levels 2 weeks before death in early infancy (age: 28 days to 3 months). We also estimated 7% to 12% risk increases for respiratory deaths per 10-microg/m3 increase in particulate matter < 10 microm in aerodynamic diameter exposure experienced 2 weeks before death for infants 4 to 12 months of age. Risk of respiratory death more than doubled for infants 7 to 12 months of age who were exposed to high average levels of particulates in the previous 6 months. Furthermore, the risk of dying as a result of sudden infant death syndrome increased 15% to 19% per 1-part per hundred million increase in average nitrogen dioxide levels 2 months before death. Low birth weight and preterm infants seemed to be more susceptible to air pollution-related death resulting from these causes; however, we lacked statistical power to confirm this heterogeneity with formal testing. Conclusions: Our results add to the growing body of literature implicating air pollution in infant death from respiratory causes and sudden infant death syndrome and provide additional information for future risk assessment.

 

Woodruff TJ, Parker JD, Schoendorf KC.
Fine particulate matter (PM2.5) air pollution and selected causes of postneonatal infant mortality in California.
Environ Health Perspect. 2006 May; 114(5):786-90.

Studies suggest that airborne particulate matter (PM) may be associated with postneonatal infant mortality, particularly with respiratory causes and sudden infant death syndrome (SIDS). To further explore this issue, we examined the relationship between long-term exposure to fine PM air pollution and postneonatal infant mortality in California. We linked monitoring data for PM<or=2.5 microm in aerodynamic diameter (PM2.5) to infants born in California in 1999 and 2000 using maternal addresses for mothers who lived within 5 miles of a PM2.5 monitor. We matched each postneonatal infant death to four infants surviving to 1 year of age, by birth weight category and date of birth (within 2 weeks). For each matched set, we calculated exposure as the average PM2.5 concentration over the period of life for the infant who died. We used conditional logistic regression to estimate the odds of postneonatal all-cause, respiratory-related, SIDS, and external-cause (a control category) mortality by exposure to PM2.5, controlling for the matched sets and maternal demographic factors. We matched 788 postneonatal infant deaths to 3,089 infant survivors, with 51 and 120 postneonatal deaths due to respiratory causes and SIDS, respectively. We found an adjusted odds ratio for a 10-microg/m3 increase in PM2.5 of 1.07 [95% confidence interval (CI): 0.93-1.24] for overall postneonatal mortality, 2.13 (95% CI, 1.12-4.05) for respiratory-related postneonatal mortality, 0.82 (95% CI, 0.55-1.23) for SIDS, and 0.83 (95% CI, 0.50-1.39) for external causes. The California findings add further evidence of a PM air pollution effect on respiratory-related postneonatal infant mortality.

 

McCallum RI.
Occupational exposure to antimony compounds.
J Environ Monit. 2005 Dec; 7(12):1245-50. E-pub 2005 Oct 26.

The toxicology of antimony and its compounds is known from three sources: its medicinal use over centuries, studies of process workers in more recent times, and more recent still, studies of its presence in modern city environments and in domestic environments. Gross exposure to antimony compounds over long periods, usually the sulfide (SbS3) or the oxide (Sb2O3) has occurred in antimony miners and in antimony process workers. There have been relatively few of these, and few studies of possible symptoms have been made. Antimony sulfide imported from, at different times, China, South Africa, and South America was processed in the North-East of England from about 1870 to 2003. The process workers in North-East England have been studied at different times, notably by Sir Thomas Oliver in 1933, and by the Newcastle upon Tyne University Department of Occupational Medicine on later occasions. Studies which have been made of the working environment, and in particular of the risk of lung cancer in process workers, have underlined the high levels of exposure to antimony compounds and to other toxic materials. However, the working conditions in antimony processing have improved markedly over the last 30 years, and the workforce had been much reduced in numbers following automation of the process. Prior to the cessation of the industry in the UK it had become a 'white coat' operation with relatively few people exposed to high concentrations of antimony. Antimony, which is normally present in domestic environments, has also been studied as a possible cause of cot death syndrome (SIDS) but extensive investigations have not confirmed this. The full importance of environmental antimony has still to be determined, and evidence of specific effects has not yet been presented.

 

Grigg J.
Gases from fossil fuel combustion: a danger to infants?
Arch Dis Child. 2005 Jul;90(7):662-3.
Comment on:
Arch Dis Child. 2005 Jul;90(7):750-3.

 

Klonoff-Cohen H, Lam PK, Lewis A.
Outdoor carbon monoxide, nitrogen dioxide, and sudden infant death syndrome.
Arch Dis Child. 2005 Jul;90(7):750-3.

AIMS: To investigate whether infants who died of SIDS were more likely to have higher acute and lifetime average exposures to outdoor carbon monoxide (CO) and nitrogen dioxide (NO2) than comparison healthy infants. METHODS: A total of 169 case and 169 matched control infants born between 1988 and 1992, were studied. CO and NO2 concentrations, averaged for all days within the infant's lifespan, and the last 30 days, 7 days, 3 days, and 1 day of life were obtained from air pollutant data provided by the California Air Resources Board. RESULTS: Based on monthly aggregated data, average CO and particularly NO2 were associated with SIDS count, even after adjustment for seasonal trends. SIDS outcome was not significantly associated with high average outdoor CO levels for any time period. However, high average outdoor NO2 levels on the last day of the infant's exposure period were significantly associated with SIDS; the adjusted odds ratio was 2.34 (95% CI 1.13 to 4.87). CONCLUSIONS: SIDS may be related to high levels of acute outdoor NO2 exposure during the last day of life. Further studies are needed to replicate this finding.

 

Nevas M, Lindstrom M, Virtanen A, Hielm S, Kuusi M, Arnon SS, Vuor Korkeala H.
Infant botulism acquired from household dust presenting as sudden infant death syndrome
J Clin Microbiol. 2005 Jan: 43(1): 511-3.

Clostridium botulinum type B was detected by multiplex PCR in the intestinal contents of a suddenly deceased 11-week-old infant and in vacuum cleaner dust from the patient's household. C. botulinum was also isolated from the deceased infant's intestinal contents and from the household dust. The genetic similarity of the two isolates was demonstrated by pulsed-field gel electrophoresis and randomly amplified polymorphic DNA analysis, thereby confirming that dust may act as a vehicle for infant botulism that results in sudden death.

---

October 2009

Accessibility  •  Copyright © Georgetown University  •  (866) 866-7437 (toll free)  •  (202) 687-7466 (local)

2115 Wisconsin Avenue, NW, Suite 601  •  Washington, DC 20007  •  info@sidscenter.org  •  (202) 784-9777 (fax)