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.

Scientists have revealed how environmental irritants such as air pollution and cigarette smoke cause people to cough, in research published today in the American Journal of Respiratory and Critical Care Medicine. The authors of the study, from Imperial College London and the University of Hull, have identified the reaction inside the lungs that can trigger coughing when a person is exposed to particular irritants in the air. They suggest that their findings may ultimately lead to the development of new treatments for chronic coughing. 

Coughing is the most common reason for people visiting a family doctor. Treatment options are limited for people with chronic coughing; a recent study concluded that over-the-counter remedies are ineffective and there is increasing concern about the safety of these therapies in children. 

Today’s study indicates, for the first time, how coughing can be triggered when a person is exposed to certain irritants in the air. It shows that the irritants can switch on receptor proteins called TRPA1 on the surface of nerve endings in the lungs. This switches on sensory nerves, which then trigger a cough reflex. The researchers say coughing could potentially be treated by blocking TRPA1 receptors, to stop irritants in the air from setting off this chain reaction. They hope that this could ultimately help millions of people whose lives are affected by chronic coughing. 

Professor Maria Belvisi, corresponding author of the study from the National Heart and Lung Institute at Imperial College London, said: “For some people, chronic coughing can be annoying and uncomfortable, but for others it can be distressing and can have a severe impact on their quality of life. Many people say that certain things in the air can make them cough and we are very excited that we have shown, for the first time, exactly what is probably happening inside the lungs. Now that we think we have cracked the mechanism, we can start investigating whether we can stop people from coughing excessively by blocking the receptor protein that triggers it.” 

To reach their conclusions, the researchers first looked at sensory nerves from mice, guinea pigs and humans, and showed that the receptors on the sensory nerves were activated by a number of irritants, including a key compound in cigarette smoke (acrolein) and a chemical called cinnamaldehyde. The researchers then blocked the receptors and showed that these substances no longer activated the nerves. 

To establish whether activating the receptor causes coughing, the researchers looked at the effect of acrolein on guinea pigs, as they have a coughing reflex. The researchers assessed the guinea pigs’ coughing after inhaling acrolein. The compound caused coughing, and the higher the concentration, the more the guinea pigs coughed. The researchers then showed that blocking the receptor using a drug significantly reduced the guinea pigs’ coughing response to the compound.

Finally, researchers led by Professor Alyn Morice at the University of Hull looked at the effect of inhaling the chemical cinnamaldehyde in humans. Ten healthy, non-smoking volunteers inhaled the chemical, as well as control substances. The researchers measured their cough response on five occasions, 2-3 days apart. All of the volunteers coughed after inhaling the compound. 

Reference: Imperial College London, Research reveals exactly how coughing is triggered by environmental irritants, November 23, 2009

Surprisingly little is known about the effects of big-city air pollution on olfactory function and even less about its effects on the intranasal trigeminal system, which elicits sensations like burning, stinging, pungent, or fresh and contributes to the overall chemosensory experience. 

Using the Sniffin’ Sticks olfactory test battery and an established test for intranasal trigeminal perception, we compared the olfactory performance and trigeminal sensitivity of residents of Mexico City, a region with high air pollution, with the performance of a control population from the Mexican state of Tlaxcala, a geographically comparable but less polluted region. 

We compared the ability of 30 young adults from each location to detect a rose-like odor (2-phenyl ethanol), to discriminate between different odorants, and to identify several other common odorants. The control subjects from Tlaxcala detected 2-phenyl ethanol at significantly lower concentrations than the Mexico City subjects, they could discriminate between odorants significantly better, and they performed significantly better in the test of trigeminal sensitivity. 

We conclude that Mexico City air pollution impairs olfactory function and intranasal trigeminal sensitivity, even in otherwise healthy young adults. 

Reference:    Guarneros M, Hummel T, Martínez-Gómez M, Hudson R., Mexico City Air Pollution Adversely Affects Olfactory Function and Intranasal Trigeminal Sensitivity, Chem Senses. 2009 Oct 9.

Growing evidence shows that exposure to lead in the environment is associated with cardiovascular disease, including increased risk of hypertension. However, those studies have looked at lead concentrations in blood, not bone lead, a better indicator of cumulative lead exposure over time. In a new study, researchers at the Harvard School of Public Health (HSPH) and the University of Michigan School of Public Health found that bone lead was associated with a higher risk of death from all causes, particularly from cardiovascular disease. It is the first study to analyze the association between bone lead and mortality.

The study appears online on September 8, 2009, on the website of the journal Circulation and will appear in a later print edition. 

“The findings with bone lead are dramatic. It is the first time we have had a biomarker of cumulative exposure to lead and the strong findings suggest that, even in an era when current exposures are low, past exposures to lead represent an important predictor of cardiovascular death, with important public health implications worldwide,” said Marc Weisskopf, assistant professor of environmental and occupational epidemiology at HSPH and lead author of the study.

Air pollution was the main source of lead in the environment in recent years, though it has been decreasing since leaded gasoline was banned in the U.S. in the mid-1990s. Most of the lead circulating in the body is deposited in bone and remains there for years, unlike blood lead, which has a half life of about 30 days. Since adverse effects from lead on the cardiovascular system would be expected to show up over time, the researchers expected that bone lead would be a better marker of chronic toxicity.

The researchers, led by Weisskopf and senior author Howard Hu, professor of environmental health, epidemiology and internal medicine at the University of Michigan School of Public Health, analyzed data from 868 participants in the Department of Veterans Affairs Normative Aging Study, a study of aging in men that began in 1963. Blood lead and bone lead—analyzed using X-ray fluorescence—were measured for each of the participants. The results showed that the risk of death from cardiovascular disease was almost six times higher in men with the highest levels of bone lead compared to men with the lowest levels. The risk of death from all causes was 2.5 times higher in men with the highest levels of lead compared to those with the lowest levels. The results appeared independent of age, smoking, education, race, alcohol, physical activity, BMI, high density lipoprotein or total cholesterol levels, hypertension or diabetes.

There are a number of mechanisms, such as increased oxidative stress, by which lead exposure may result in cardiovascular mortality, say the authors. They also note that, in addition to high blood pressure, exposure to lead has been associated with widened pulse-pressure (an indicator of arterial stiffening) and heart disease.

Given that bone lead may be a better biomarker of cumulative lead exposure than blood lead, it may be the best predictor of chronic disease from exposure to lead in the environment. “In addition to spurring further public health measures to reduce exposure to lead and to begin monitoring for cumulative exposure, mechanistic and clinical research is needed to determine if opportunities exist to conduct targeted screening and treatment that can further reduce the burden of cardiovascular disease for the millions of adults who have had years of elevated lead exposure in the past,” said Hu.

Reference:    Harvard School of Public Health, Lead in bone associated with increased risk of death from cardiovascular disease in men, Boston, MA, September 9, 2009

Air pollution as a potential contributor of disease

There has been remarkable progress over the past 20years in pushing forward our understanding of many facets of autoimmune disease. Indeed, knowledge of the genetic basis of autoimmunity and the molecular and cellular pathways involved in its pathogenesis has reached an unprecedented level. Yet this knowledge has not served to prevent autoimmune disease nor to curtail the dramatic rise in its incidence over the same interval. Population-level genetic changes cannot explain this trend; thus, environmental factors are strongly implicated. Among the possible environmental contributors to autoimmune disease, air pollution exposure has received very little attention. Although there is only a small amount of published data directly examining a possible causal relationship between air pollution exposure and autoimmunity, data from related fields suggests that it could facilitate autoimmunity as well. If correct, this hypothesis could prove to have sizeable public health implications. 

Reference:   Ritz SA, Air pollution as a potential contributor to the ‘epidemic’ of autoimmune disease, Medical Sciences Division, Northern Ontario School of Medicine, East Campus – Laurentian University, Med Hypotheses. 2009 Aug 7.