Printer Friendly

Does particulate air pollution contribute to infant death? A systematic review.

There is now substantial evidence that both short- and long-term increases in ambient air pollution are associated with increased mortality and morbidity in adults and children. Children's health is particularly vulnerable to environmental pollution, and infant mortality is still a major contributor to childhood mortality. In this systematic review we summarize and evaluate the current level of epidemiologic evidence of an association between particulate air pollution and infant mortality. We identified relevant publications using database searches with a comprehensive list of search terms and other established search methods. We included articles in the review according to specified inclusion criteria. Fifteen studies met our inclusion criteria. Evidence of an association between particulate air pollution and infant mortality in general was inconsistent, being reported from locations with largely comparable pollution levels. There was some evidence that the strength of association with particulate matter differed by subgroups of infant mortality. It was more consistent for postneonatal mortality due to respiratory causes and sudden infant death syndrome. Differential findings for various mortality subgroups within studies suggest a stronger association of particulate air pollution with some causes of infant death. Research is needed to confirm and clarify these links, using the most appropriate methodologies for exposure assessment and control of confounders. Key words: infant mortality, particulate air pollution, postneonatal respiratory mortality, sudden infant death syndrome, systematic review. Environ Health Perspect 112:1365-1370 (2004). doi: 10.1289/ehp.6857 available via http://dx.doi.org/[Online 3 June 2004]

**********

The historic 1952 pollution episode in London, when a rapid increase in smog led to dramatic increases in daily mortality, including infant mortality (Her Majesty's Public Health Service 1954), stimulated early studies into the effect of air pollution on population health. There is now widespread evidence that short-term increases in ambient air pollution increase mortality and morbidity in adults and children, even at exposure levels below the World Health Organization (WHO) Air Quality Guidelines for Europe, and U.S. Environmental Protection Agency (EPA) standards (Brunekreef et al. 1995; Committee on the Medical Effects of Air Pollution 1998; Dockery and Pope 1994; Holgate et al. 1999; Katsouyanni et al. 1997; Kunzli et al. 2000; Lebowitz 1996; Pope et al. 1995; Samet et al. 2000; Schwartz 1994a; Sydbom et al. 2001; U.S. EPA 1987; WHO 1987). The findings are particularly consistent for particulate air pollution; most of the current evidence is available for inhalable particulate air pollution [particulate matter (PM) with a 50% cutoff aerodynamic diameter < 10 [micro]m (P[M.sub.10]) and < 2.5 [micro]m (P[M.sub.2.5])] (Dominici et al. 2003; Katsouyanni et al. 1997). The effects were found to be stronger in susceptible population groups, such as the elderly, young children, and people with preexisting cardiovascular and respiratory conditions (Gouveia and Fletcher 2000; Pope 2000; Saldiva et al. 1995; Schwartz 1994b). Long-term exposure to particulate air pollution has also been associated with increases in total mortality and in cardiopulmonary mortality and respiratory morbidity (European Environment Agency 2003; Pope 2000; Pope et al. 1995). The large overall impact of air pollution on human health and a nonthreshold linear relationship with some health outcomes (e.g., mortality and hospital admission) have prompted the WHO to put air pollution and its health effects on its agenda. It also led the U.S. EPA to draft its 2003 criteria document, which forms the basis for reevaluating the current U.S. ambient air quality standards for PM (U.S. EPA 2003; WHO 2002).

The health of infants and children is particularly vulnerable to environmental pollution and is the focus of the recently published European Environment and Health Strategy (European Comission 2003). Infant mortality remains the major contributor to childhood mortality worldwide, despite significant declines over the last two decades. Infant mortality rates vary considerably across regions and population groups, and the reasons for this variation are not fully understood. Environmental exposures, including ambient air pollution, may account partly for excesses in infant deaths. We undertook a systematic review to summarize the epidemiologic evidence for an association between levels of particulate air pollution and infant outcomes. This work was part of a broader systematic review of the association between ambient air pollution and fetal (Glinianaia et al. 2004) and infant health outcomes.

Materials and Methods

Identification of publications and review process. Our methods were based on the guidelines published by the U.K. National Health Service Centre for Reviews and Dissemination (2001). We identified relevant publications using database searches with a comprehensive list of search terms and other established search methods (for details, see Glinianaia et al. 2004).

The inclusion criteria for articles were a) nonaccidental exposure to directly measured PM; b) an infant (during the first year of life) health outcome; c) publication between 1 January 1966 and 31 December 2003 in the English language; and d) availability through the British Library (London, UK) or the Internet. Articles describing outcomes related to occupational or accidental exposure were excluded, as were articles that were available as abstracts only. Only one relevant article on infant morbidity was identified by our comprehensive literature search (Gehring et al. 2002); all others explored infant mortality as an infant health outcome.

Those articles meeting the inclusion criteria were appraised by pairs of reviewers using a piloted data extraction form based on previous reviews (Bell et al. 1998; Rankin et al. 1998). We extracted information on study design, measurement methods for pollutants and outcomes, statistical techniques, confounding factors, and results.

Exposure measurements. Most reviewed studies used total suspended particulates (TSP) (Bobak and Leon 1992, 1999b; Chay and Greenstone 1999, 2003; Ha et al. 2003; Hunt and Cross 1975; Joyce et al. 1989; Lave and Seskin 1972; Penna and Duchiade 1991; Shinkura et al. 1999), P[M.sub.10] (Lipfert et al. 2000; Woodruff et al. 1997), or P[M.sub.2.5] (Gehring et al. 2002; Loomis et al. 1999) as measures of exposure to PM. One study used visibility as a measure of particulate air pollution (Knobel et al. 1995). Where possible, we recalculated effect estimates (odds and risk ratios, mean changes) as the expected change in outcome for an increase in air pollution levels by 10 [micro]g/[m.sup.3] (TSP, P[M.sub.10], P[M.sub.2.5]). This facilitated comparison across studies using the same particle size measurements.

Infant mortality. The following definitions were used as reported in the studies: Infant mortality is the number of deaths within the first year of life per 1,000 live births; neonatal mortality (NM), the number of neonatal deaths within 0-27 days of life per 1,000 live births; postneonatal mortality (PNM), the number of deaths between 28 days and 1 year of life per 1,000 live births (Bobak and Leon 1992, 1999b; Lipfert et al. 2000) or per 1,000 neonatal survivors (Woodruff et al. 1997). Infant deaths are conventionally divided into neonatal and postneonatal deaths. The underlying causes of death differ in these time periods; in particular, preterm birth is the largest contributor to neonatal death (Maternal and Child Health Research Consortium 2001). Many reviewed studies also categorized mortality by cause of death (definitions are given in Table 1).

Study design. A study was described as ecologic if both outcome and exposure data were measured at a geographic area-based level. A study was described as time series when an ecologic study was based in one geographically defined population with data collected at different points in time. In semi-individual studies (cohort, case-control, and cross-sectional), outcome data were collected at an individual level and air pollution data were measured at an area-based level.

Although considered, a meta-analysis was not undertaken due to the heterogeneity of methodologies used in the studies. The results are summarized narratively with 95% confidence intervals (CIs) for estimates where possible. Given the different ways in which the studies have reported results, we could consistently report only whether any association or difference was statistically significant at the 5% level.

Results

Study methods. Fifteen studies met our inclusion criteria, and the findings of the 14 articles addressing mortality are summarized in Table 1. Key aspects of study quality (i.e., study design, sample size, control for confounders) are also reported. Table 1 gives estimates unadjusted for other pollutants because there was no consistency as to whether associations with PM were reported after adjustment for other pollutants.

The studies varied by design, geographic setting, PM source and composition, copollutant exposures, exposure period investigated, and outcome. Ten studies were ecologic or time series (Bobak and Leon 1992; Chay and Greenstsone 1999, 2003; Ha et al. 2003; Joyce et al. 1989; Knobel et al. 1995; Lave and Seskin 1972; Loomis et al. 1999; Penna and Duchiade 1991; Sinkura et al. 1999), two were cross-sectional (Hunt and Cross 1975; Lipfert et al. 2000), two were cohort studies (Gehring et al. 2002; Woodruff et al. 1997), and one a matched case-control study (Bobak and Leon 1999b). All used area-based estimates of air pollution exposure, except for the German study, which used a Geographic Information Systems model to provide individual ambient pollution estimates (Gehring et al. 2002). Thirteen studies used direct measurements of PM from routine monitoring of the ambient air pollution level by monitoring stations in the study areas (Bobak and Leon 1992, 1999b; Chay and Greenstone 1999, 2003; Ha et al. 2003; Hunt and Cross 1975; Joyce et al. 1989; Lave and Seskin 1972; Lipfert et al. 2000; Loomis et al. 1999; Penna and Duchiade 1991; Sinkura et al. 1999; Woodruff et al. 1997), and one study used visibility as a measure of particulate air pollution, which was reported to be highly correlated with P[M.sub.10] levels (Knobel et al. 1995).

Five of the ecologic and time-series studies used the annual mean concentrations of particles (Bobak and Leon 1992; Chay and Greenstone 1999, 2003; Lave and Seskin 1972; Penna and Duchiade 1991), whereas the others used means over other periods (Joyce et al. 1989; Shinkura et al. 1999) or investigated different periods before death (Ha et al. 2003; Knobel et al. 1995; Loomis et al. 1999). In the case-control study, exposure was assigned as the mean of all 24-hr particulate air pollution measurements for the period between birth and death of the index case (Bobak and Leon 1999b), whereas in the U.S. cohort study, the mean of the PM levels for the first 2 months of life was used (Woodruff et al. 1997). In the two cross-sectional studies, the exposure period was not specified in one (Hunt and Cross 1975), whereas the other used the annual mean of P[M.sub.10] (Lipfert et al. 2000). In the German cohort study on respiratory morbidity, the estimated annual averages of P[M.sub.2.5] were used (Gehring et al. 2002).

Adjustments for some maternal and socioeconomic factors were made by a number of studies (Table 1); a few also adjusted for maternal smoking (Gehring et al. 2002; Lipfert et al. 2000; Woodruff et al. 1997), other air pollutants (Bobak and Leon 1992, 1999b; Lipfert et al. 2000; Loomis et al. 1999), and/or season/ weather (Chay and Greenstone 1999; Ha et al. 2003; Knobel et ah 1995; Lave and Seskin 1972). One older cross-sectional study did not adjust for any confounding factors (Hunt and Cross 1975). Considering the comparative precision of the exposure measurements and the adjustment for key confounding factors in mortality studies, the Czech case-control study (Bobak and Leon 1999b) and the U.S. cohort study (Woodruff et al. 1997) used the strongest designs, and their results are highlighted in the findings below.

Study findings. Mortality outcomes: infant mortality. The eight studies exploring PM and total infant mortality found little evidence of a consistent association (Table 1). Five studies of varying designs reported some positive associations (Chay and Greenstone 2003; Hunt and Cross 1975; Lave and Seskin 1972; Lipfert et al. 2000; Loomis et al. 1999), although the strength of evidence and critical exposure period differed. Three other studies (Bobak and Leon 1999b; Chay and Greenstone 1999; Penna and Duchiade 1991) reported nonsignificant associations. The case-control study (Bobak and Leon 1999b) found little evidence of any association with TSP levels [odds ratio (OR) = 1.03; 95% CI, 0.99-1.06].

The three studies investigating infant mortality due to respiratory causes reported a significant association with PM (Bobak and Leon 1999b; Lipfert et al. 2000; Penna and Duchiade 1991) but used different measures of effects. The case-control study (Bobak and Leon 1999b) reported a weak association with TSP levels (OR = 1.12; 95% CI, 1.01-1.28). These three studies also reported total infant mortality, and the strength of association was consistently lower than for respiratory mortality, although no formal comparisons were made.

The single study reporting infant mortality due to nonrespiratory causes found no significant association between PM levels and mortality due to this cause (Bobak and Leon 1999b) (OR = 1.01; 95% CI, 0.98-1.05), in contrast to their more positive findings for respiratory mortality.

Neonatal mortality. Total NM did not show a consistent association with PM, with one U.S. study reporting a positive association (Lipfert et al. 2000), two studies with borderline findings (Bobak and Leon 1992; Chay and Greenstone 1999), and five studies from different geographic settings reporting no evidence of an association (Bobak and Leon 1999b; Chay and Greenstone 2003; Joyce et al. 1989; Lave and Seskin 1972; Shinkura et al. 1999).

The case-control study was the only one to explore NM due to both respiratory and nonrespiratory causes. It reported little evidence of an association between TSP levels and either type of NM: respiratory, OR = 0.93 (95% CI, 0.67-1.32); nonrespiratory, OR = 1.00 (95% CI, 0.96-1.06) (Bobak and Leon 1999b). Another study examining respiratory NM reported a significant association with P[M.sub.10] similar in strength to the association reported for total NM (Lipfert et al. 2000).

Postneonatal mortality. Four of five studies investigating a relationship between PM and total PNM, including a cohort study (OR = 1.04; 95% CI, 1.02-1.07) (Woodruff et al. 1997), reported significant positive associations (Bobak and Leon 1992; Ha et al. 2003; Lipfert et al. 2000). The case-control study did not find a significant association (OR = 1.04; 95% CI, 0.99-1.10) (Bobak and Leon 1999b); the difference between this and the cohort study was in the precision of the estimates. Two (Bobak and Leon 1999b; Lipfert et al. 2000) of the five studies explored PNM in addition to total infant and total NM and reported similar strengths of association for all these mortality types.

In all studies examining both total and respiratory PNM (Bobak and Leon 1992, 1999b; Ha et al. 2003; Lipfert et al. 2000; Woodruff et al. 1997), the association between PM level and respiratory mortality was statistically significant and stronger than for total mortality, although no formal comparisons were made. This was true for infants of normal birth weight in the cohort study, but the results were inconclusive for the subgroup of infants with low birth weight (Woodruff et al. 1997). In the two studies where both postneonatal respiratory and nonrespiratory mortalities were investigated, there was little evidence of an association between PM levels and nonrespiratory mortality (Bobak and Leon 1999b; Woodruff et al. 1997).

Sudden infant death syndrome (SIDS) was found to be associated with ambient PM concentrations in two U.S. studies (Lipfert et al. 2000; Woodruff et al. 1997). A Taiwanese time-series study found a positive association between SIDS and reduced visibility during 1-9 days before death (Knobel et al. 1995), but adjustment for confounders was limited. Although the U.S. cohort study found a significant association with P[M.sub.10] (OR = 1.12; 95% CI, 1.07-1.17), the Czech case-control study did not find a significant association with TSP (OR = 0.91; 95% CI, 0.75-1.12) (Bobak and Leon 1999b).

Morbidity outcomes: respiratory morbidity. The only study investigating respiratory morbidity in infants reported significant associations between exposure to P[M.sub.2.5] and some (cough without infection and dry cough at night) but not other (wheeze, asthmoid or other types of bronchitis, respiratory infections, and sneezing, runny/stuffed nose) respiratory symptoms (Gehring et al. 2002).

Discussion

Main findings. Our review suggests some evidence of an association between PM levels and different subgroups of infant mortality. There were differences in the magnitude and consistency of association by cause of death, with PNM due to respiratory causes and SIDS being more consistently associated with PM levels. However, it is problematic to compare cause-specific associations between studies because of variations in definitions and diagnostic criteria of causes of death. Differential findings for various mortality subgroups within some studies suggest a stronger association of particulate air pollution with some causes of infant death. The only study investigating respiratory morbidity in infants reported significant associations between exposure to P[M.sub.2.5] and some but not other respiratory symptoms (Gehring et al. 2002).

Methodologic issues. We were unable to take publication, language, and reporting biases into account when identifying relevant publications, which may have overestimated the strength of any associations.

Summarizing the findings was complicated by the considerable differences in methodologies used. Many articles reported the results relating to a number of combinations of PM, outcome, and exposure period, resulting in multiple comparisons, which in turn increased the likelihood of positive findings.

More than half of the reviewed studies were ecologic or time series in design. Controlling for confounding factors in such studies is more difficult than in individual-based studies because of the extra potential sources of bias due to the aggregation of subjects into groups (Morgenstern and Thomas 1993). Even in semi-individual studies, few adjusted for key confounding factors at an individual level, because some used area-based level data and others did not adjust for confounders. Other important individual risk factors, such as smoking and environmental exposures from other air pollutants (e.g., sulfur dioxide, nitrogen dioxide), were rarely controlled for. Adequate control for confounders is essential to accurately estimate the magnitude of any association between low-level particulate air pollution exposure and infant health, and inadequate control may partly account for some inconsistency between studies.

Air pollution exposure was generally estimated by small numbers of monitors, which may not estimate individual exposures accurately for all infants; this could result in misclassification of exposure. The potential for bias is also affected by monitoring decisions (e.g., annual or daily means). The absence of information about indoor air pollution may underestimate individual exposure. These factors are likely to be nondifferential and therefore reduce the precision of effect estimates.

Studies exploring the health effects of PM may report inconsistent results because the definitions and measurement techniques are variable. The toxicity of equal-sized PM depends on its chemical composition, which, in turn, depends on the mixture of sources generating them and their dispersion (Mage 2002). For example, the P[M.sub.10]: TSP ratio ranges from 50 to 60% for U.S. sampling sites (Dockery and Pope 1994), whereas in the Czech Republic P[M.sub.10] has been estimated to constitute about 80% of TSP (Bobak and Leon 1999a). The reviewed studies also varied in relation to average levels and ranges of PM, and copollutant exposures. Despite differences in air pollution sources and levels, the findings of an association between PM levels and postneonatal respiratory mortality are fairly consistent across studies and regions.

Another possible explanation for inconsistency of findings is differences between settings in the distribution of timing and cause of death within infant mortality. For instance, the definitions of respiratory causes of death and SIDS varied across studies (Bobak and Leon 1992, 1999b; Knobel et al. 1995; Lipfert et al. 2000; Woodruff et al. 1997) and were not always fully reported (Lipfert et al. 2000). Accurate diagnosis of deaths due to SIDS depends on a postmortem investigation, and this was not available for all cases coded as SIDS in one study (Knobel et al. 1995). For this reason, within-study comparisons, when different subgroups and causes of death were examined in the same study, may be more valid than between-study comparisons.

The magnitudes of association reported in the reviewed studies are low and could be accounted for by the factors considered above. However, their magnitude is of the same order as that found between PM and adult mortality, which is accepted as a true relationship (Committee on the Medical Effects of Air Pollution 1998; WHO 2002).

Potential mechanisms. Although the epidemiologic evidence linking increases in PM with excess mortality and morbidity in adults is now strong, the mechanisms for such a link are not yet well understood. To date, toxicologic studies have not identified unequivocally specific PM constituents or mechanisms to account for the epidemiologic observations. Infants and children are considered potentially susceptible populations in risk assessments, including risk from PM (U.S. EPA 1999), because of their immature immune system, potential impact on lung growth and development, and viral infections common in infants. However, few human and animal studies have compared immature and adult organisms with regard to their susceptibility to inhaled particles (Mauderly 2000). For adults, three potential mechanisms have been put forward for the PM effect: an inflammatory response that alters blood coagulation, an allergic immune response, and an alteration in cardiac autonomic function resulting in the reduction of heart rate variability (Donaldson et al. 2001; Granum and Lovik 2002; Liao et al. 2004; Pope 2000). All three potential mechanisms may be pertinent in infants, but the degree of their influence may vary at various stages of infant development. In particular, they may be more applicable to postneonatal death, because this is thought to be affected more by the infant's external environment than is NM (Pharoah and Morris 1979). Neonatal deaths are more affected by conditions originating in the perinatal period, with immaturity-related conditions being the main cause of death. However, if there is a small adverse effect of particulate air pollution on fetal growth and duration of pregnancy, as discussed previously (Glinianaia et al. 2004), it may also indirectly contribute to neonatal deaths.

The mechanisms of SIDS, the most common cause of postneonatal death in developed countries, are not well understood, although a number of pathways have been proposed. One of the currently most compelling hypotheses for the occurrence of SIDS is an abnormality of brain development and maturation, with a tendency to central apnea and disturbed cardiorespiratory control mechanisms (Goldwater 2003; Harper 2000; Kahn et al. 2003; Kinney and Filiano 2001). Unsafe sleeping environment, exposure to environmental tobacco smoke (ETS), and lower socioeconomic status are critical risk factors for SIDS. It has been suggested that the association between postnatal exposure to tobacco smoke and SIDS is causal (Anderson and Cook 1997; McMartin et al. 2002). The potential mechanisms of action proposed for ETS (abnormal pulmonary development, reduced pulmonary function, abnormalities in cardiorespiratory control system, promotion of respiratory infections) (Chan-Yeung and Dimich-Ward 2003; Goldwater 2003; Hoflauis et al. 2003; Strachan and Cook 1997) might be similar to those for particulate air pollution, because ETS is known to contain a substantial proportion of PM.

Implications. Current epidemiologic evidence suggests a link between ambient PM exposure and some subgroups of infant mortality, even at relatively low PM levels reported in the reviewed studies, which are comparable with current levels experienced in developed countries. More research is needed to further clarify whether there is a real effect of particulate air pollution on infant health and to quantify this effect. Future studies should explore overall and cause-specific infant mortality, using robust study designs with individual level information on key confounding variables. Exposure assessment should include details of level, size, and composition of PM and co-pollution exposure. The use of physiologic measurements (e.g., lung function in older children) and biomarkers of exposure or effect (e.g., methemoglobin as a biomarker of carbon monoxide poisoning, cotinine as a marker of exposure to ETS, placental DNA adduct levels as biomarkers of effect of polycyclic aromatic hydrocarbons) could promote understanding of causal effects of air pollution on infant and children's health. If a causal association between exposure to PM and infant death exists, widespread exposure to particulate air pollution may be an important determinant of infant mortality at a population level.

REFERENCES

Anderson HR, Cook DO. 1997. Passive smoking and sudden infant death syndrome: review of the epidemiological evidence. Thorax 52:1003-1009.

Bell R, Luengo S, Petticrew M, Sheldon T. 1998. Screening for ovarian cancer: a systematic review. Health Tech Assess 2:1-84.

Bobak M, Leon DA. 1992. Air pollution and infant mortality in the Czech Republic, 1986-88. Lancet 340:1010-1014.

Bobak M, Leon DA. 1999a. Pregnancy outcomes and outdoor air pollution: an ecological study in districts of the Czech Republic 1986-8. Occup Environ Med 56:539-543.

Bobak M, Leon DA. 1999b. The effect of air pollution on infant mortality appears specific for respiratory causes in the postneonatal period. Epidemiology 10:666-670.

Brunekreef B, Dockery DW, Krzyzanowski M. 1995. Epidemiologic studies on short-term effects of low levels of major ambient air pollution components. Environ Health Perspect 103:3-13.

Chan-Yeung M, Dimich-Ward H. 2003. Respiratory health effects of exposure to environmental tobacco smoke. Respirology 8:131-139.

Chay KY, Greenstone M. 1999. The Impact of Air Pollution on Infant Mortality: Evidence from Geographic Variation in Pollution Shocks Induced by a Recession. Working paper W 7442. Cambridge, MA: National Bureau of Economic Research.

Chay KY, Greenstone M. 2003. Air Quality, Infant Mortality, and the Clean Air Act of 1970. Working paper W 10053. Cambridge, MA: National Bureau of Economic Research.

Committee on the Medical Effects of Air Pollution. 1998. The Quantification of the Effects of Air Pollution on Health in the United Kingdom. London: Her Majesty's Stationery Office.

Dockery DW, Pope CA III 1994. Acute respiratory effects of particulate air pollution. Annu Rev Public Health 15:107-132.

Dominici F, McDermott A, Daniels M, Zeger SL, Samet JM. 2003. Mortality among residents of 90 cities. In: Revised Analyses of Time-Series Studies of Air Pollution and Health (Lament J, ed). Boston: Health Effects Institute, 9 24. Available: http:// www.healtheffects.org/Pubs/TimeSeries.pdf [accessed 29 April 2004].

Donaldson K, Stone V, Seaton A, MacNee W. 2001. Ambient particle inhalation and the cardiovascular system: potential mechanisms. Environ Health Perspect 109:523-527.

European Commission. 2003. A European Environment and Health Strategy. Brussels: European Commission, 11 June. Available: http://europa.eu.int/comm/pressroom/presapacks/pdf/ com_en.pdf [accessed 22 October 2003].

European Environment Agency. 2003. Environment and human health. In: Europe's Environment: The Third Assessment. Report No. 10. Copenhagen: European Environment Agency. Available: http://reports.eea.euJnt/environmental assessment_report_2003_10/en/kiev_chapt12.pdf [accessed 22 October 2003].

Gehring U, Cyrys J, Sedlmeir 6, Brunekreef B, Bellander T, Fischer P, et al. 2002. Traffic-related air pollution and respiratory health during the first 2 years of life. Eur Respir J 19:690-698.

Glinianaia SV, Rankin J, Bell R, Pless-Mulloli T, Howel D. 2004. Particulate air pollution and fetal health: a systematic review of the epidemiologic evidence. Epidemiology 15:36-45.

Goldwater PN. 2003. Sudden infant death syndrome: a critical review of approaches to research. Arch Dis Child 88:1095-1100.

Gouveia N, Fletcher T. 2000. Time series analysis of air pollution and mortality: effects by cause, age and socioeconomic status. J Epidemiol Commun Health 54:750-755.

Granum B, Lovik M. 2002. The effect of particles on allergic immune responses. Toxicol Sci 65:7-17.

Ha EH, Lee JT, Kim H, Hong YC, Lee BE, Park HS, et al. 2003. Infant susceptibility of mortality to air pollution in Seoul, South Korea. Pediatrics 111:284-290.

Harper RM. 2000. Sudden infant death syndrome: a failure of compensatory cerebellar mechanisms? Pediatr Res 48:140-142.

Her Majesty's Public Health Service. 1954. Mortality and Morbidity during the London Fog of December 1952. Reports on Public Health and Medical Subjects. London: Her Majesty's Stationery Office.

Hofhuis W, de Jongste JC, Merkus PJ. 2003. Adverse health effects of prenatal and postnatal tobacco smoke exposure on children. Arch Dis Child 88:1086-1090.

Holgate ST, Samet JM, Koren HS, Maynard RL, eds. 1999. Air Pollution and Health. London: Academic Press.

Hunt VR, Cress WL 1975. Infant mortality and the environment of a lesser metropolitan county: a study based on births in one calendar year. Environ Res 9:135-151.

Joyce TJ, Grossman M, Goldman E. 1989. An assessment of the benefits of air pollution control: the case of infant health. J Urban Econ 25:32-51.

Kahn A, Groswasser J, France P, Scaillet S, Sawaguchi T, Kelmanson I, et al. 2003. Sudden infant deaths: stress, arousal and SIDS. Early Hum Dev 75:S147-S166.

Katsouyanni K, Touloumi G, Spix C, Schwartz J, Balducci F, Medina S, et al. 1997. Short-term effects of ambient sulphur dioxide and particulate matter on mortality in 12 European cities: results from time series data from the APHEA project. Br Med J 314:1658-1663.

Kinney HC, Filiano JJ. 2001. Brain research in sudden infant death syndrome. In: Sudden Infant Death Syndrome: Problems, Progress and Possibilities (Byard RW, Krouse HF, eds). London: Arnold, 118 137.

Knobel HH, Chen CJ, Liang KY. 1995. Sudden infant death syndrome in relation to weather and optimetrically measured air pollution in Taiwan. Pediatrics 96:1106-1110.

Kunzli N, Kaiser R, Medina S, Studnicka M, Chanel O, Filliger P, et al. 2000. Public-health impact of outdoor and traffic-related air pollution: a European assessment. Lancet 356:795-801.

Lave LB, Seskin EP. 1972. Air pollution, climate, and home heating: their effects on U.S. mortality rates. Am J Public Health 62:909-916.

Lebowitz MD. 1996. Epidemiological studies of the respiratory effects of air pollution. Eur Respir J 9:1029-1054.

Liao D, Duan Y, Whitsel EA, Zheng ZJ, Heiss G, Chinchilli VM, et al. 2004. Association of higher levels of ambient criteria pollutants with impaired cardiac autonomic control: a population-based study. Am J Epidemiol 159:768-777.

Lipfert FW, Zhang J, Wyzga RE. 2000. Infant mortality and air pollution: a comprehensive analysis of US data for 1990. J Air Waste Manage Assoc 50:1350-1366.

Loomis O, Castillejos M, Gold DR, McDonnell W, Borja-Aburto VH. 1999. Air pollution and infant mortality in Mexico City. Epidemiology 10:118-123.

Mage DT. 2002. A particle is not a particle is not a PARTICLE. J Expo Anal Environ Epidemiol 12:93-95.

Maternal and Child Health Research Consortium. 2001. Confidential Enquiry into Stillbirths and Deaths in Infancy (CESOI) 8th Annual Report: Focusing on Stillbirths, European Comparisons of Perinatal Care, Paediatric Portmortem Issues, Survival Rates of Premature Babies--Project 27/28. London: Maternal and Child Health Research Consortium.

Mauderly JL. 2000. Animal models for the effect of age on susceptibility to inhaled particulate matter. Inhal Toxicol 12:863-900.

McMartin KI, Platt MS, Hackman R, Klein J, Smialek JE, Vigorito R, et al. 2002. Lung tissue concentrations of nicotine in sudden infant death syndrome (SIDS). J Pediatr 140:205-209.

Morgenstern H, Thomas D. 1993. Principles of study design in environmental epidemiology. Environ Health Perspect 101:23-38.

National Health Service Centre for Reviews and Dissemination. 2001. Undertaking Systematic Reviews of Research on Effectiveness: CRD's Guidance for Those Carrying Gut or Commissioning Reviews. Report No. 4 (2nd ed). York, UK: Centre for Reviews and Dissemination.

Penna ML, Duchiade MP. 1991. Air pollution and infant mortality from pneumonia in the Rio de Janeiro metropolitan area. Bull Pan Am Health Organ 25:47-54.

Pharoah PO, Morris JN. 1979. Postneonatal mortality. Epidemiol Rev 1:170-183.

Pope CA III. 2000. Epidemiology of fine particulate air pollution and human health: biologic mechanisms and who's at risk? Environ Health Perspect 108:713-723.

Pope CA III, Bates DV, Raizenne ME. 1995. Health effects of particulate air pollution: time for reassessment? Environ Health Perspect 103:472-480.

Rankin J, Carlin L, White M. 1998. A Review of the Literature on Interventions to Reduce Mortality from Breast and Cervical Dancer in Minority Ethnic Groups. London: Cancer Research Campaign.

Saldiva PH, Pope CA III, Schwartz J, Dockery DW, Lichtenfels A J, Salge JM, et al. 1995. Air pollution and mortality in elderly people: a time-series study in Sao Paulo, Brazil. Arch Environ Health 50:159-163.

Samet JM, Dominici F, Curriero FC, Coursac I, Zeger SL. 2000. Fine particulate air pollution and mortality in 20 U.S. cities, 1987 1994. N Engl J Med 343:1742-1749.

Schwartz J. 1994a. Air pollution and daily mortality: a review and meta analysis. Environ Res 64:36-52.

Schwartz J. 1994b. What are people dying of on high air pollution days? Environ Res 64:26-35.

Shinkura R, Fujiyama C, Akiba S. 1999. Relationship between ambient sulfur dioxide levers and neonatal mortality near the Mt. Sakurajima volcano in Japan. J Epidemiol 9: 344-349.

Strachan DP, Cook DG. 1997. Health effects of passive smoking. 1. Parental smoking and lower respiratory illness in infancy and early childhood. Thorax 52:905-914.

Sydbom A, Blomberg A, Parnia S, Stenfors N, Sandstrom T, Dahlen SE. 2001. Health effects of diesel exhaust emissions. Eur Respir J 17:733-746.

U.S. EPA. 1987. Ambient Air Quality Standards for Particulate Matter: Final Rules. Fed Reg 52:24634-24655.

U.S. EPA. 1999. Air Quality Criteria for Particulate Matter, vols. 1-3. EPA/800/P-99/002a. Washington, DC: U.S. Environmental Protection Agency.

U.S. EPA. 2003. Air Quality Criteria for Particulate Matter. Fourth External Review Draft, June 2003. Research Triangle Park, NC: U.S. Environmental Protection Agency, Office of Research and Development, National Center for Environmental Assessment.

Woodruff TJ, Grille J, Schoendorf KC. 1997. The relationship between selected causes of postneonatal infant mortality and particulate air pollution in the United States. Environ Health Perspect 105:608-612.

WHO. 1977. International Statistical Classification of Diseases, Injuries, and Causes Of Death, 9th Revision. Geneva: World Health Organization.

WHO 1987. Air Quality Guidelines for Europe. WHO Regional Publications, European Series No. 23. Copenhagen: World Health Organization.

WHO. 2002. Reducing Risks, Promoting Healthy Life. The World Health Report 2002. Geneva: World Health Organization. Available: http://www.who.int/whr/2002/en/ [accessed 20 October 2003].

Svetlana V. Glinianaia, Judith Rankin, Ruth Bell, Tanja

Pless-Mulloli, and Denise Howel

Public Health Research Group, School of Population and Health Sciences,

Faculty of Medical Sciences, University of Newcastle, Newcastle upon

Tyne, United Kingdom

Address correspondence to S.V. Glinianaia, School of Population and Health Sciences, Faculty of Medical Sciences, University of Newcastle, Newcastle upon Tyne, NE2 4HH, United Kingdom. Telephone: 0191-222-5891. Fax: 0191-222-8211. E-mail: svetlana.glinianaia@ncl.ac.uk

The major part of the work on this review was supported by funds from the School of Population and Health Sciences (Epidemiology and Public Health), University of Newcastle. Additional literature searching and reviewing of articles published in 2002-2003 and revision to the manuscript in response to reviewers' comments were supported by Wellcome Trust grant 072465/Z/03/Z.

The authors declare they have no competing financial interests.

Received 12 November 2003; accepted 3 June 2004.
COPYRIGHT 2004 National Institute of Environmental Health Sciences
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2004, Gale Group. All rights reserved. Gale Group is a Thomson Corporation Company.

Article Details
Printer friendly Cite/link Email Feedback
Title Annotation:Children's Health / Review
Author:Howel, Denise
Publication:Environmental Health Perspectives
Date:Oct 1, 2004
Words:5787
Previous Article:Acute infections and environmental exposure to organochlorines in inuit infants from Nunavik.
Next Article:Drinking-water nitrate, methemoglobinemia, and global burden of disease: a discussion.
Topics:


Related Articles
Air pollution is a serious cardiovascular risk.
Air pollution and adverse pregnancy outcomes: response.
Association of air pollution with increased incidence of ventricular tachyarrhythmias recorded by implanted cardioverter defibrillators.
Burning Atlanta: all the old regulatory weapons couldn't reform the Georgia power plant that is America's single biggest polluter. But a new law is...
Fine particulate matter national ambient air quality standards: public health impact on populations in the northeastern United States.
A case-crossover study of wintertime ambient air pollution and infant bronchiolitis.
Fine particulate matter (P[M.sub.2.5]) air pollution and selected causes of postneonatal infant mortality in California.
Gaseous air pollutants and hospitalization for respiratory disease in the neonatal period.
Low-level ozone exposure and respiratory symptoms in infants.

Terms of use | Privacy policy | Copyright © 2019 Farlex, Inc. | Feedback | For webmasters