Air pollution and emergency room visits for asthma in Santa Clara County, California.

Abstract

During the winters of 1986-1987 through 1991-1992, rainfall throughout much of Northern California was subnormal, resulting in intermittent accumulation of air pollution, much of which was attributable to residential wood combustion (RWC). This investigation examined whether there was a relationship between ambient air pollution in Santa Clara County, California and emergency room visits for asthma during the winters of 1988-1989 through 1991-1992. Emergency room (ER) records from three acute-care hospitals were abstracted to compile daily visits for asthma and a control diagnosis (gastroenteritis) for 3-month periods during each winter. Air monitoring data included daily coefficient of haze (COH) and every-other-day particulate matter with aerodynamic diameter equal to or less than 10 microns (PM10, 24-hr average), as well as hourly nitrogen dioxide and ozone concentrations. Daily COH measurements were used to predict values for missing days of PM10 to develop a complete PM10 time series. Daily data were also obtained for temperature, precipitation, and relative humidity. In time-series analyses using Poisson regression, consistent relationships were found between ER visits for asthma and PM10. Same-day nitrogen dioxide concentrations were also associated with asthma ER visits, while ozone was not. Because there was a significant interaction between PM10 and minimum temperature in this data set, estimates of relative risks (RRs) for PM10-associated asthma ER visits were temperature-dependent. A 60 micrograms/m3 change in PM10 (2-day lag) corresponded to RRs of 1.43 (95% CI = 1.18-1.69) at 20 degrees F, representing the low end of the temperature distribution, 1.27 (95% CI = 1.13-1.42) at 30 degrees F, and 1.11 (95% CI = 1.03-1.19) at 41 degrees F, the mean of the observed minimum temperature. ER visits for gastroenteritis were not significantly associated with any pollutant variable. Several sensitivity analyses, including the use of robust regressions and of nonparametric methods for fitting time trends and temperature effects in the data, supported these findings. These results demonstrate an association between ambient wintertime PM10 and exacerbations of asthma in an area where one of the principal sources of PM10 is RWC.ImagesFigure 1.

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“…An increase of PM 10 results in a greater use of asthma medication, frequent visits to medical practitioners and increase of asthma-related hospital admissions (Schwartz et al, 1993;Lipsett et al, 1997;Peters et al, 1997;Atkinson et al, 1999;Norris et al, 1999, Delfino et al, 2002Maciejczyk et al, 2004, Monteil, 2008Yeatts et al, 2009;Scapellato et al, 2009). In these studies the association between asthma attacks and different triggers as such as PM 10 , ozone (O 3 ), nitrogen dioxide (NO 2 ), sulfur dioxide (SO 2 ), and carbon monoxide (CO) have been investigated.…”

“…In these studies the association between asthma attacks and different triggers as such as PM 10 , ozone (O 3 ), nitrogen dioxide (NO 2 ), sulfur dioxide (SO 2 ), and carbon monoxide (CO) have been investigated. Some reported significant correlations between asthma-related hospital admissions and concentrations of PM 10 and NO 2 (Lipsett et al, 1997), PM 10 and SO 2 and/or SO 4 (Peters et al, 1997;Atkinson et al, 1999) or PM 2.5 or PM 10 and CO (Norris et al, 1999;Sheppard et al, 1999) whereas others, using multi-pollutant models, contend that asthma is related to PM concentrations only (Nauenberg and Basu, 1999;Tolbert et al, 2000). All studies that used single-pollutant models have reported significant association of particles and asthma admissions (Schwartz et al, 1992;Maciejczyk et al, 2004;Monteil, 2008;Scapellato et al, 2009).…”

“…All studies that used single-pollutant models have reported significant association of particles and asthma admissions (Schwartz et al, 1992;Maciejczyk et al, 2004;Monteil, 2008;Scapellato et al, 2009). In spite of ozone being considered as an asthma trigger itself some studies indicate that both PM 10 and O 3 are associated with increases in asthma (Karin et al, 2009), whereas others disagree with this notion (Lipsett et al, 1997;Atkinson et al, 1999;Nauenberg and Basu, 1999). Note that high pollution episodes are largely governed by local conditions, high O 3 levels are typical of the summer (generated by photochemical reactions between oxides of nitrogen and volatile organic compounds VOC) and elevated PM 10 levels may occur during the summer or winter (as in Arizona and California for example).…”

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“…[11,12]. The response of airway cells to these stimuli is mediated through activation of distinct transmembrane signaling intermediates [13].…”

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“…There are many studies which link exposure to air pollution, and specifically particulate matter (PM), with increased morbidity and mortality due to respiratory illnesses, such as asthma 1 , 2 , 3 , 4 bronchiolitis 5 , 6 and chronic obstructive pulmonary disease 7 , 8 , 9 . These epidemiological studies generally focus on relating mortality and hospital admissions for respiratory or cardiac conditions to a broad range of “general” PM, including particles originating from soil and other natural sources, “road‐dust” from tyre and brake wear, and diesel exhaust particles (DEP).…”