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Date: October 25, 1999
To: Ed Murphy, Project Manager
From: Poki Namkung, M.D., M.P.H., Health Officer

That the Commission recommend that the City Council approve continuing air quality studies consisting of a series of real-time measurements of PM10 during the evening rush hour in various weather conditions and seasons.

On October 7, 1999, I received a request to review the data regarding air quality at the proposed Harrison Street playing fields in relation to community concern about the prevalence of asthma. My analysis of these issues includes a review of the 1997 Acurex Environmental air quality study, a review of the medical literature on the association of asthma and inhalation of particulate matter and discussion with physicians at the California Environmental Protection Agency.

In this report, I will briefly present the pathophysiology of asthma; the epidemiological data linking ambient particulate matter (PM) to severa1 measures of asthma exacerbation including hospital admissions, emergency room visits and altered lung function; and finally, a recommendation.

In reviewing the Acurex study, two issues immediately surfaced. First, the two major mobile sources of pollutants, 1-880 and the railway have both experienced increased volumes of traffic and trains since the study was done in 1997. Secondly, the fine particulate matter (PM10) readings were close to the standard established by the California EPA (50 ug/m3, 24-hr AAQS). This pollutant was not considered in the acute or chronic exposure hazard risk assessment.

In discussions with physicians in the Office of Environmental Health Hazard Assessment, California Environmental Protection Agency, I learned that a standard considered more protective of children of 30 ug/m3, 24hr AAQS will be proposed in accordance with SB25, the Children's Environmental Protection Law just signed by Governor Davis. Since two major sources of particulate matter had increased in volume since the study was done, the existing measurement is no longer accurate. In addition, in the intervening two years since the study was done, significantly more is known about the relationship between particulate matter and asthma.

Asthma is a chronic respiratory disease with three primary features: airway inflammation, altered epithelial function associated with mucin hypersecretion and altered immunological response, and, most importantly, recurrent airflow obstruction. It is characterized by intermittent episodes of wheezing, coughing and breathlessness. Asthma is a multifactorial disease associated with familial, infectious, allergenic, socioeconomic, psychosocial and environmental factors.

Asthma is the most common chronic disease affecting children and young adults in the United States. It is probably the only common treatable condition whose prevalence, severity and mortality is increasing, despite advances in therapy. In the United States in 1998 it is estimated that 173 million persons (4.8 million of these are children) had asthma as compared to 6.7 million total persons in 1980.

Prevalence studies from 1988 to 1992 have found that between 4%-12% of children in the United States have doctor-diagnosed asthma. Comparisons of prevalence survey data between 1973 and 1986 in Britain show a 6.9% increase in prevalence in boys and 12.8% increase in girls. Worth noting is the designation of doctor-diagnosed asthma in these prevalence studies. A recent study of 214 high school varsity football players found that 9% had exercise induced bronchospasms, a serious form of airway obstruction that is typical of asthma. None of the 214 players had ever been diagnosed with asthma.

Assuming that varsity football requires a level of athleticism and talent that would preclude breathing problems leads to the possible conclusion that the undiagnosed natural prevalence of asthma in children would be much higher than what is reported.

The hallmark of asthma is considered nonspecific airway hyper reactivity or bronchial hyper responsiveness. This hyper responsiveness refers to an enhanced tendency of the airways to constrict in response to a variety of chemical and physical stimuli. While the cause or causes of asthma is unknown, much is known about the stimuli that trigger asthma. In particular, there is a growing body of epidemiological evidence of the association between PM exposure and exacerbation of asthma.

Particulate matter may exacerbate asthma through several mechanisms that may not be mutually exclusive:

  1. reflex brorichoconstriction via a nonspecific irritant effect;
  2. direct toxicity to the airway epithelium and resident immune cells;
  3. induction of an inflammatory immune response.

Several toxicology studies in nonasthmatic humans and animals have demonstrated this inflammatory response. Thus far, tests have not been performed on asthmatic subjects presumably because this effect can be induced in normal subjects as opposed to hyperreactive subjects.

Numerous studies have consistently observed associations between air pollution and mortality. A constant finding in these studies is the order of the relative strengths of the associations between mortality and specific criteria pollutants. These pollutants can be ranked from strongest to weakest as follows: PM2.5> PM10 >SOx > H+> 03 > NOx. (PM2. Inhalable particles of less than 2.5-um aerodynamic diameter; PM10 - Inhalable particles of less than 10-um aerodynamic diameter; SO - sulfur oxides; H+ - hydrogen ions; Os - ozone; N0 - nitrous oxides)  In most recent studies, PM is the dominant pollutant and the strength of this relationship is remarkably consistent across studies. Although the composition of PM10 may be site specific, typically, particles in the 2.5-to 10-um size range consist of re-entrained road dust (soil particles, engine oil including metals, tire particles, sulfate arid nitrate).

The quantitative effects of PM on asthma outcomes as reported by epidemiological studies are reported as follows. These adverse health outcomes reflect exacerbation of asthma and include hospital admissions, emergency room visits, and increases in asthma symptoms.

The PM concentrations were measured over one to two seasons per year or monthly during the time period of the study, depending on the study model. Hospital admissions and emergency room visits were measured daily over periods of seasons or years, depending on the study model. Exacerbation of symptoms were measured daily, weekly or by doctor visit depending on the study model. A summary of the results:

• Hospital admissions: range of PM10 measured (mean, ug/m3) 3O-54; range of percent increase in admissions = 6% - 26%

• Emergency Room Visits: range of PM10 10-46; range of percent increase in ER visits = 5.6%-100%

• Exacerbation of symptoms: range of PM10 46->100; range of percent increase in symptoms 23%-80%

Meta-analysis of these studies reveals that the most likely range of effects of a 10-ug/m3 increase of PM over baseline will result in an increase in asthma symptoms of 4-5%.

All of the above studies involve the effects of acute exposure. One additional study examines the effects of long-term exposure to PM2.5 and PM 10 on the severity of symptoms related to asthma. This study looked at a cohort of Seventh Day Adventists and found that higher long-term exposure to PM2.5 and PM10 was associated with worsening in general asthma status. The effect was not quantified in this study.

In conclusion, all of the studies in the literature on the association of inhalation of particulate matter and asthma provide evidence for coherence of effects across a wide range of adverse outcomes. I find the Acurex study lacking in several aspects:

1) Only two measurements of PM were done on days when weather conditions did not approximate potential worst case scenarios.
2) No analysis of the acute or chronic exposure hazards of PM was done
3) The measurements were done before the increase in rail and freeway traffic that exists today.

My recommendation is the following: A series of real-time measurements of PM10 during the evening rush hour in various weather conditions and seasons. Should these new air quality studies reveal sub-standard conditions, these results must be disseminated such that people could make an informed judgment about individual risk.

Finally, to place this entire issue of air quality into a real world context, people do live, work and play in areas with far worse air quality than this proposed site. Given the potential range of readings from new air quality studies, there is no doubt that there will be some increased morbidity in respiratory disease, either acute or chronic, reported or not, for children playing at this proposed site. How much of an increase is for policy makers and the public to hammer out. Any physician, honoring their oath, would have to state that no increase in morbidity is acceptable. However in the real world, is it better for children to have access to organized sports activities when fully one quarter of our children are sedentary and almost one third are clinically obese?

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