California’s dirty air caused more than $193 million in hospital-based medical care from 2005 to 2007 as people sought help for problems such as asthma and pneumonia that are triggered by elevated pollution levels, according to a new RAND Corporation study.

Researchers estimate that exposure to excessive levels of ozone and particulate pollution caused nearly 30,000 emergency room visits and hospital admissions over the study period. Public insurance programs were responsible for most of the costs, with Medicare and Medi- Cal covering more than two-thirds of the expenses, according to the report.

“California’s failure to meet air pollution standards causes a large amount of expensive hospital care,” said John Romley, lead author of the study and an economist at RAND, a nonprofit research organization. “The result is that insurance programs — both those run by the government and private payers — face higher costs because of California’s dirty air.”

While much work has been done previously to catalog the economic impact of air pollution across California, the RAND study is the first to quantify the cost of hospital-based medical care to various payers caused by the failure to meet federal clean air standards across the state. More people in California live in areas that do not meet federal clean air standards than in any other state.

Romley said the findings show that private insurers, employers and public insurance programs all have a financial stake in improving California’s air quality.

“These costs may not be the largest problem caused by dirty air, but our study provides more evidence about the impact that air pollution has on the state’s economy,” Romley said.

Researchers used records from air pollution agencies and hospitals to estimate how failing to meet federal and state standards for particulate matter and ozone would affect private and public insurer spending for hospital admissions for respiratory and cardiovascular causes, and emergency room visits for asthma throughout California from 2005-2007.

Researchers say the most common hospital-based medical care triggered by elevated air pollution levels are emergency room visits for asthma among children aged 17 and under, with more than 12,000 visits over the three-year study period.

The most costly conditions examined by researchers were hospital admissions triggered by air pollution for acute bronchitis, pneumonia and chronic obstructive pulmonary disease. Those conditions accounted for nearly one-third of the $193 million in health care spending documented over the study period.

Nearly three-quarters of the health events identified by researchers were triggered by high levels of fine particulate pollution — tiny pieces of soot that can lodge deep in lungs. The health events examined in the study were concentrated in the San Joaquin Valley and the four-county South Coast Air Basin.

The cost of treating health events caused by air pollution is equal to the expense of providing flu vaccines to 85 percent of California children under age 15, according to the report.

Researchers say their study provides a conservative estimate about the costs of medical care triggered by air pollution because it does not include outpatient care provided in clinics or medical offices. Details about that type of medical care are not routinely reported to state agencies and thus could not be analyzed.

The study also includes case studies of individual hospitals in Fresno, Lynwood, Palo Alto, Riverside and Sacramento. That analysis demonstrates that costs and types of illness reported vary by region.

To conduct the study, researchers used epidemiological studies that link elevated pollution levels to respiratory and cardiovascular illnesses, and compared that information to pollution levels measured across the state from 2005 to 2007 by various public agencies. Researchers also reviewed detailed records hospitals report to the state about the patients they treat, the illnesses diagnosed and who pays for that care.

Literature:

RAND Corporation*, Study finds dirty air in California causes millions worth of medical care each year, March 2, 2010

*The RAND Corporation is a nonprofit research organization providing objective analysis and effective solutions that address the challenges facing the public and private sectors around the world.

New York State (NYS) employees who responded to the World Trade Center (WTC) disaster on or after 11 September 2001 potentially experienced exposures that might have caused persistent respiratory effects. NYS responders represent a more moderately exposed population than typical first responders. 

To assess whether NYS employees who were WTC responders were more likely than controls to report lower respiratory symptoms (LRS) or a diagnosis of asthma 5 years post-9/11, persistence and severity of symptoms were also evaluated. 

Participants were initially mailed self-administered questionnaires (initial, Year 1, Year 2) and then completed a telephone interview in Year 3. Data were analysed using Poisson’s regression models. 

WTC exposure was associated with LRS, including cough symptoms suggestive of chronic bronchitis, 5 years post-9/11. When exposure was characterized using an exposure assessment method, the magnitude of effect was greater in those with exposure scores above the mean. WTC exposure was associated with persistence of LRS over the 3 year study period. Results also suggest that participants with the highest exposures were more likely to experience increased severity of their asthma condition and/or LRS. 

The findings suggest that even in a moderately exposed responder population, lower respiratory effects were a persistent problem 5 years post-9/11, indicating that some WTC responders require ongoing monitoring.  

Literature: Mauer MP, Cummings KR, Hoen R., Long-term respiratory symptoms in World Trade Center responders, Bureau of Occupational Health, Center for Environmental Health, New York State Department of Health, Occup Med (Lond). 2009 Dec 24.

The prevalence of allergic diseases such as asthma and pollinosis is steadily increasing and seems to be associated with modern lifestyle. Therefore, it has been hypothesized that high living standards and hygienic conditions reduce exposure to microbial components, and lead to an imbalance in the immune system, especially in the Thl and Th2 system, which increases the risk for the development of allergic diseases.

However, recent accumulated epidemiological evidences have demonstrated that air pollutants including diesel exhaust particulate (DEP) and NO2 are responsible for the increased prevalence of allergies. The effects of environmental chemicals have also been supported by the in vivo and in vitro studies. It is important to prevent allergy development in our life as early as possible (e.g., since our infancy). 

Reference: Nakamura H, Hitomi Y., Environmental factors in allergic diseases, Kanazawa University, Nippon Rinsho. 2009 Nov;67(11):2043-7.

The prevalence of allergies and asthma among the world’s population has been steadily increasing due to environmental factors. 

 It has been described that exposure to ozone, diesel exhaust particles, or tobacco smoke exacerbates allergic inflammation in the lungs. These environmental oxidants increase the levels of cellular reactive oxygen species (ROS) and induce mitochondrial dysfunction in the airway epithelium. 

In this study, we investigated the involvement of preexisting mitochondrial dysfunction in the exacerbation of allergic airway inflammation. After cellular oxidative insult induced by ragweed pollen extract (RWE) exposure, we have identified nine oxidatively damaged mitochondrial respiratory chain-complex and associated proteins. Out of these, the ubiquinol-cytochrome c reductase core II protein (UQCRC2) was found to be implicated in mitochondrial ROS generation from respiratory complex III. Mitochondrial dysfunction induced by deficiency of UQCRC2 in airway epithelium of sensitized BALB/c mice prior the RWE challenge increased the Ag-induced accumulation of eosinophils, mucin levels in the airways, and bronchial hyperresponsiveness. Deficiency of UQCRC1, another oxidative damage-sensitive complex III protein, did not significantly alter cellular ROS levels or the intensity of RWE-induced airway inflammation. 

These observations suggest that preexisting mitochondrial dysfunction induced by oxidant environmental pollutants is responsible for the severe symptoms in allergic airway inflammation. These data also imply that mitochondrial defects could be risk factors and may be responsible for severe allergic disorders in atopic individuals. 

Reference:  Aguilera-Aguirre L, Bacsi A, Saavedra-Molina A, Kurosky A, Sur S, Boldogh I., Mitochondrial Dysfunction Increases Allergic Airway Inflammation, J Immunol. 2009 Sep 28.

The fact that only some individuals exposed to environmental chemicals develop chemical intolerance raises the possibility that genetic factors could be contributing factors. The present communication summarizes evidence from a genetic animal model of cholinergic supersensitivity that suggests that an abnormal cholinergic system could be one predisposing genetic factor.

The Flinders Sensitive Line (FSL) rats were established by selective breeding for increased responses to an organophosphate. It was subsequently found that these FSL rats were also more sensitive to direct-acting muscarinic agonists and had elevated muscarinic receptors compared to the selectively bred parallel group, the Flinders Resistant Line (FRL) rats, or randomly bred control rats.

Increased sensitivity to cholinergic agents has also been observed in several human populations, including individuals suffering from chemical intolerance. Indeed, the FSL rats exhibit certain behavioral characteristics such as abnormal sleep, activity, and appetite that are similar to those reported in these human populations. In addition, the FSL rats have been reported to exhibit increased sensitivity to a variety of other chemical agents. Peripheral tissues, such as intestinal and airway smooth muscle, appear to be more sensitive to both cholinergic agonists and an antigen, ovalbumin. Hypothermia, a centrally mediated response, is more pronounced in the FSL rats after nicotine and alcohol, as well as agents that are selective for the dopaminergic and serotonergic systems.

In some cases, the increased sensitivity has been detected in the absence of any changes in the receptors with which the drugs interact (dopamine receptors), while receptor changes have been seen in other cases (nicotine receptors). Therefore, there may be multiple mechanisms underlying the multiple chemical sensitivity-chemical intolerance of the FSL rats. An elucidation of these mechanisms may provide useful clues to those involved in chemical intolerance in humans. 

Reference: Overstreet DH, Djuric V., A genetic rat model of cholinergic hypersensitivity: implications for chemical intolerance, chronic fatigue, and asthma, University of North Carolina, Ann N Y Acad Sci. 2001 Mar;933:92-102.