Name : Putri Kilaswari Winarto
Class : XI.2 perawat
Article I
Air pollution increases risk of autism by 50 percent in newborns
(NaturalNews) A recent study by the California Department of Health Services indicates that industrial air pollutants may increase the risk of autism by 50 percent in young children and unborn babies. The report was published online in the journal Environmental Health Perspectives.
Researchers compared 959 children from six San Francisco Bay area counties who were born in 1994. Out of these, 284 were diagnosed with autism-spectrum disorders. The study showed that children with autism were more likely to be born in areas with high levels of mercury, cadmium, nickel, trichloroethylene and vinyl chloride. Elemental mercury -- which is released into the air from coal-burning power plants, chlorine factories and gold mines -- appears to be particularly hazardous.
In their report, the study authors said their research suggests "living in areas with higher ambient levels of hazardous air pollutants -- particularly metals and chlorinated solvents -- during pregnancy or early childhood, may be associated with a moderately increased risk of autism. These findings illuminate the need for further scientific investigation, as they are biologically plausible but preliminary and require confirmation."
Mercury levels are increasing in many parts of the world, and over the past 10 years the number of children diagnosed with autism has increased as well. This leads many scientists to suspect there may be a connection between pollutants and the neurological disorder. However, the study's lead author Gayle Windham cautions that more definitive evidence is needed before scientists will have a clear understanding of the effect of environmental pollutants on autism.
Summary
Paragraph 1 : industrial air pollutants can increase the risk of autism by 50 percent in children and unborn babies.
Paragraph 2 : children with autism are more likely to be born in areas with high levels of mercury, cadmium, nickel, vinyl chloride, and trichloroethylene.
Paragraph 3 : live in areas with higher ambient levels of hazardous air pollutants during pregnancy or early childhood, may be associated with risk of autism is increasing.
Paragraph 4 : more definitive evidence is needed before scientists will have a clear understanding of the environmental effect of pollutants on autism.
Article II
Exposure To Environmental Tobacco Smoke Causes Respiratory Symptoms In Healthy Adults
Over time, inhaling environmental tobacco smoke (ETS)--a process often called "passive smoking"--can cause otherwise healthy adults to develop chronic respiratory symptoms.
The findings appear in the second issue for November 2006 of the American Journal of Respiratory and Critical Care Medicine, published by the American Thoracic Society.
Margaret W. Gerbase, Ph.D., of the Division of Pulmonary Medicine at the University Hospitals of Geneva in Switzerland, and 11 associates assessed the respiratory symptoms in 1,661 never-smokers over an 11-year period. All individuals in the study cohort participated in the Swiss Study on Air Pollution and Lung Diseases in Adults in 1991 and again in 2002. The two-part study was the first large-scale investigation of the long-term health effects of moderate ambient air pollution in Switzerland.
"The results of our longitudinal assessment of ETS effects in asymptomatic never-smokers showed that exposure to ETS was associated with the development of respiratory symptoms," said Dr. Gerbase. "A particularly strong effect of continued exposure to ETS was observed among previously asymptomatic individuals with bronchial hyper-reactivity."
The researchers found ETS exposure to be strongly associated with the development of cough. In subjects with bronchial hyper-reactivity, they observed a link between ETS and symptoms like wheeze, cough, dyspnea (shortness of breath) and chronic bronchitis. However, only the association between dyspnea and ETS reached statistical significance.
According to the authors, individuals with bronchial hyper-reactivity who are persistently exposed to ETS are at particular risk of developing early-onset chronic respiratory disease. "Symptom development in our subjects was accompanied by decrements in spirometric indices reflecting peripheral airway narrowing, notably in subjects with bronchial hyper-responsiveness," said Dr. Gerbase.
Of the 1,661 participants, 1,202 individuals (72.4 percent) reported never being exposed to ETS, 309 persons (18.6 percent) reported exposure only during the 1991 survey, and 150 subjects (9 percent) reported exposure both in 1991 and 2002.
"Indirect evidence derived from smokers shows that airway responsiveness increases the risk to develop cough, phlegm, dyspnea and chronic bronchitis," said Dr. Gerbase. "Cessation of smoking leads to remission of symptoms and improvement in airway hyper-reactivity."
Excluded from participation in the study at baseline (1991) were all potential participants who reported such symptoms as wheeze, cough, phlegm, dyspnea and chronic bronchitis, or who were taking a medication for asthma at the time.
The researchers concluded that their findings support the need for policies protecting all nonsmokers from the "detrimental effects" of ETS.a
The findings appear in the second issue for November 2006 of the American Journal of Respiratory and Critical Care Medicine, published by the American Thoracic Society.
Margaret W. Gerbase, Ph.D., of the Division of Pulmonary Medicine at the University Hospitals of Geneva in Switzerland, and 11 associates assessed the respiratory symptoms in 1,661 never-smokers over an 11-year period. All individuals in the study cohort participated in the Swiss Study on Air Pollution and Lung Diseases in Adults in 1991 and again in 2002. The two-part study was the first large-scale investigation of the long-term health effects of moderate ambient air pollution in Switzerland.
"The results of our longitudinal assessment of ETS effects in asymptomatic never-smokers showed that exposure to ETS was associated with the development of respiratory symptoms," said Dr. Gerbase. "A particularly strong effect of continued exposure to ETS was observed among previously asymptomatic individuals with bronchial hyper-reactivity."
The researchers found ETS exposure to be strongly associated with the development of cough. In subjects with bronchial hyper-reactivity, they observed a link between ETS and symptoms like wheeze, cough, dyspnea (shortness of breath) and chronic bronchitis. However, only the association between dyspnea and ETS reached statistical significance.
According to the authors, individuals with bronchial hyper-reactivity who are persistently exposed to ETS are at particular risk of developing early-onset chronic respiratory disease. "Symptom development in our subjects was accompanied by decrements in spirometric indices reflecting peripheral airway narrowing, notably in subjects with bronchial hyper-responsiveness," said Dr. Gerbase.
Of the 1,661 participants, 1,202 individuals (72.4 percent) reported never being exposed to ETS, 309 persons (18.6 percent) reported exposure only during the 1991 survey, and 150 subjects (9 percent) reported exposure both in 1991 and 2002.
"Indirect evidence derived from smokers shows that airway responsiveness increases the risk to develop cough, phlegm, dyspnea and chronic bronchitis," said Dr. Gerbase. "Cessation of smoking leads to remission of symptoms and improvement in airway hyper-reactivity."
Excluded from participation in the study at baseline (1991) were all potential participants who reported such symptoms as wheeze, cough, phlegm, dyspnea and chronic bronchitis, or who were taking a medication for asthma at the time.
The researchers concluded that their findings support the need for policies protecting all nonsmokers from the "detrimental effects" of ETS.a
Summary
1. secondhand smoke can cause healthy adults to develop chronic respiratory symptoms.
2. The results of our longitudinal assessment of ETS effects in asymptomatic never-smokersshowed that exposure to
3. was associated with the development of respiratory symptoms
4. the association between dyspnea and ETS reached statistical significance.
5. individuals with bronchial hyper-reactivity who are persistently exposed to ETS are at particular risk of developing early-onset chronic respiratory disease.
6. smokers shows that airway responsiveness increases the risk to develop cough, phlegm, dyspnea and chronic bronchitis
7. Cessation of smoking leads to remission of symptoms and improvement in airway hyper-reactivity.
Article III
Higher Heart Attack Risk Associated With Increased Pollution Levels
Research published on bmj.com today revealed that high levels of pollution could increase the risk of having a heart attack for up to six hours after exposure, however, the risk diminishes after a six hour time frame.
Researchers speculate that the heart attack would have happened regardless and was merely pulled forward by a few hours. They base their assumption on the transient nature of the increased risk known as a short-term displacement (or "harvesting") effect of pollution.
Although research has proven that high pollution levels are linked to premature death from heart disease, according to the authors, the association with an increased risk of heart attack is less clear.
Krishnan Bhaskaran, an epidemiologist from the London School of Hygiene and Tropical Medicine, and his team conducted a study in which they evaluated 79,288 heart attack cases from 2003 to 2006 and hourly exposure to pollution levels.
By using the UK National Air Quality Archive they investigated the levels of specific pollutants in the atmosphere, including pollutant particles (PM10), carbon monoxide (CO), nitrogen dioxide (NO2), sulphur dioxide (SO2) and ozone.
Bhaskaran stated that higher levels of PM10 and NO2 are well-known markers of traffic related pollution.
Seeing that there was no net increase in heart attack risk over a broader timescale, the authors argue that there may be:
Researchers speculate that the heart attack would have happened regardless and was merely pulled forward by a few hours. They base their assumption on the transient nature of the increased risk known as a short-term displacement (or "harvesting") effect of pollution.
Although research has proven that high pollution levels are linked to premature death from heart disease, according to the authors, the association with an increased risk of heart attack is less clear.
Krishnan Bhaskaran, an epidemiologist from the London School of Hygiene and Tropical Medicine, and his team conducted a study in which they evaluated 79,288 heart attack cases from 2003 to 2006 and hourly exposure to pollution levels.
By using the UK National Air Quality Archive they investigated the levels of specific pollutants in the atmosphere, including pollutant particles (PM10), carbon monoxide (CO), nitrogen dioxide (NO2), sulphur dioxide (SO2) and ozone.
Bhaskaran stated that higher levels of PM10 and NO2 are well-known markers of traffic related pollution.
Seeing that there was no net increase in heart attack risk over a broader timescale, the authors argue that there may be:
"limited potential for reducing the overall burden of myocardial infarction through reductions in pollution alone, but that should not undermine calls for action on air pollution, which has well established associations with broader health outcomes including overall, respiratory and cardiovascular mortality."
Professor Richard Edwards and Dr Simon Hales from the University of Otago in New Zealand say in an accompanying editorial that:
Professor Richard Edwards and Dr Simon Hales from the University of Otago in New Zealand say in an accompanying editorial that:
"despite the strengths of the study, it is possible that a true effect was missed because of imprecise measurements and inadequate statistical power. Given other evidence that exposure to air pollution increases overall mortality and morbidity, the case for stringent controls on pollutant levels remains strong."
Summary
1. high levels of pollution could increase the risk of having a heart attack for up to six hours after exposure
2. the heart attack would have happened regardless and was merely pulled forward by a few hours.
3. the association with an increased risk of heart attack is less clear
4. higher levels of PM10 and NO2 are well-known markers of traffic related pollution.
5. limited potential for reducing the overall burden of myocardial infarction through reductions in pollution alone
6. possible that a true effect was missed because of imprecise measurements and inadequate statistical power
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