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      Fine Particulate Matter (PM 2.5) Air Pollution and Selected Causes of Postneonatal Infant Mortality in California

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          Abstract

          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 ≤2.5 μm in aerodynamic diameter (PM 2.5) to infants born in California in 1999 and 2000 using maternal addresses for mothers who lived within 5 miles of a PM 2.5 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 PM 2.5 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 PM 2.5, 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−μg/m 3 increase in PM 2.5 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.

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          Most cited references17

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          Association of fine particulate matter from different sources with daily mortality in six U.S. cities.

          Previously we reported that fine particle mass (particulate matter [less than and equal to] 2.5 microm; PM(2.5)), which is primarily from combustion sources, but not coarse particle mass, which is primarily from crustal sources, was associated with daily mortality in six eastern U.S. cities (1). In this study, we used the elemental composition of size-fractionated particles to identify several distinct source-related fractions of fine particles and examined the association of these fractions with daily mortality in each of the six cities. Using specific rotation factor analysis for each city, we identified a silicon factor classified as soil and crustal material, a lead factor classified as motor vehicle exhaust, a selenium factor representing coal combustion, and up to two additional factors. We extracted daily counts of deaths from National Center for Health Statistics records and estimated city-specific associations of mortality with each source factor by Poisson regression, adjusting for time trends, weather, and the other source factors. Combined effect estimates were calculated as the inverse variance weighted mean of the city-specific estimates. In the combined analysis, a 10 microg/m(3) increase in PM(2.5) from mobile sources accounted for a 3.4% increase in daily mortality [95% confidence interval (CI), 1.7-5.2%], and the equivalent increase in fine particles from coal combustion sources accounted for a 1.1% increase [CI, 0.3-2.0%). PM(2.5) crustal particles were not associated with daily mortality. These results indicate that combustion particles in the fine fraction from mobile and coal combustion sources, but not fine crustal particles, are associated with increased mortality.
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            Defining the sudden infant death syndrome (SIDS): deliberations of an expert panel convened by the National Institute of Child Health and Human Development.

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              The effect of ambient carbon monoxide on low birth weight among children born in southern California between 1989 and 1993.

              B Ritz, F Yu (1999)
              We evaluated the effect of carbon monoxide (CO) exposures during the last trimester of pregnancy on the frequency of low birth weight among neonates born 1989-1993 to women living in the Los Angeles, California, area. Using birth certificate data for that period, we assembled a retrospective cohort of infants whose mothers resided within 2 miles of 1 of 18 CO monitoring stations. Based on the gestational age and birth date of each child, we estimated last-trimester exposure by averaging the corresponding 3 months of daily CO concentrations registered at the monitoring station closest to the mother's residence (determined from the birth certificate). Where data were available (at 6 stations), we also averaged measurements taken daily for nitrogen dioxide and ozone and those taken at 6-day intervals for particulate matter [less than/equal to]10 microm (PM10) to approximate last-trimester exposures to other pollutants. Overall, the study cohort consisted of 125,573 singleton children, excluding infants born before 37 or after 44 weeks of gestation, those weighing below 1,000 or above 5,500 g at birth, those for whom fewer than 10 days of CO measurements were available during the last trimester, and those whose mothers suffered from hypertension, diabetes, or uterine bleeding during pregnancy. Within the cohort, 2,813 (2.2%) were low in birth weight (between 1,000 and 2,499 g). Exposure to higher levels of ambient CO (>5.5 ppm 3-month average) during the last trimester was associated with a significantly increased risk for low birth weight [odds ratio (OR) = 1.22; 95% confidence interval (CI), 1.03-1.44] after adjustment for potential confounders, including commuting habits in the monitoring area, sex of the child, level of prenatal care, and age, ethnicity, and education of the mother.
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                Author and article information

                Journal
                Environ Health Perspect
                Environmental Health Perspectives
                National Institute of Environmental Health Sciences
                0091-6765
                May 2006
                13 January 2006
                : 114
                : 5
                : 786-790
                Affiliations
                [1 ] Office of Policy, Economics, and Innovation, U.S. Environmental Protection Agency, San Francisco, California, USA
                [2 ] National Center for Health Statistics, Hyattsville, Maryland, USA
                Author notes

                Address correspondence to T.J. Woodruff, U.S. Environmental Protection Agency, 75 Hawthorne St. PPA-1, San Francisco, CA 94105 USA. Telephone: (415) 947–4277. Fax: (415) 947–3519. E-mail: woodruff.tracey@ 123456epa.gov

                The authors declare they have no competing financial interests.

                Article
                ehp0114-000786
                10.1289/ehp.8484
                1459937
                16675438
                bb27a91e-7f26-4e80-8df9-28a207d881b4
                This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original DOI.
                History
                : 10 July 2005
                : 12 January 2006
                Categories
                Research
                Children's Health

                Public health
                particulate matter air pollution,pm2.5,infant mortality,air pollution,postneonatal
                Public health
                particulate matter air pollution, pm2.5, infant mortality, air pollution, postneonatal

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