Asthma risk and acetaminophen
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Acetaminophen, causes asthma, liver failure, & male infertility,
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Asthma risk and acetaminophen
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With daily use of acetaminophen the risk of asthma increased 238%.  Other studies going back until 1991 have found a positive association.   

Thorax 2000;55:266-270 doi:10.1136/thorax.55.4.266

Frequent paracetamol use and asthma in adults


BACKGROUND The pulmonary antioxidant glutathione may limit airway inflammation in asthma. Since paracetamol (acetaminophen) depletes the lung of glutathione in animals, a study was undertaken to investigate whether frequent use in humans was associated with asthma.

METHODS Information was collected on the use of analgesics as part of a population based case-control study of dietary antioxidants and asthma in adults aged 16–49 years registered with 40 general practices in Greenwich, South London. The frequency of use of paracetamol and aspirin was compared in 664 individuals with asthma and in 910 without asthma. Asthma was defined by positive responses to questions about asthma attacks, asthma medication, or waking at night with shortness of breath. The association between analgesic use and severity of disease amongst asthma cases, as measured by a quality of life score, was also examined.

RESULTS Paracetamol use was positively associated with asthma. After controlling for potential confounding factors the odds ratio for asthma, compared with never users, was 1.06 (95% CI 0.77 to 1.45) in infrequent users (<monthly), 1.22 (0.87 to 1.72) in monthly users, 1.79 (1.21 to 2.65) in weekly users, and 2.38 (1.22 to 4.64) in daily users (p (trend) = 0.0002). This association was present in users and non-users of aspirin and was stronger when cases with more severe disease were compared with controls; amongst cases increasing paracetamol use was associated with more severe disease. Frequency of aspirin use was not associated with asthma when cases as a whole were compared with controls, nor with severity of asthma amongst cases. Frequent paracetamol use was positively associated with rhinitis, but aspirin use was not.

CONCLUSIONS Frequent use of paracetamol may contribute to asthma morbidity and rhinitis in adults.


International Journal of Epidemiology, Oxford Journals Medicine International Journal of Epidemiology Volume39, Issue3 Pp. 790-794  http://ije.oxfordjournals.org/content/39/3/790.short

Prenatal paracetamol exposure and asthma: further evidence against confounding


Background Observational studies have reported an association between maternal use of paracetamol in pregnancy and childhood asthma, which was not explained by measured confounding factors. However, it is possible that this relation might be confounded by unmeasured behavioural factors linked to paracetamol usage; if that were the case, effects of similar magnitude of partner’s paracetamol use and/or postnatal maternal use would be expected.

Methods In the Avon Longitudinal Study of Parents and Children (ALSPAC), a population-based birth cohort, we compared the univariate effects of maternal use of paracetamol in pregnancy on risk of doctor-diagnosed asthma, wheeze and elevated immunoglobulin E (IgE) in the offspring at 7 years of age, with the univariate effects of partner’s use and postnatal maternal use on these phenotypes.

Results Maternal use of paracetamol in pregnancy was strongly associated with all outcomes. Partner’s use was very weakly associated with asthma but not associated with wheezing or IgE. Postnatal maternal use was associated with asthma and wheezing, though less strongly than was prenatal use, and was not associated with IgE. On mutual adjustment, the effects of maternal use in pregnancy on all outcomes were not substantially attenuated, whereas the effects of partner’s use on asthma, and of postnatal maternal use on asthma and wheezing, were reduced.

Conclusions These findings suggest that the relation between maternal use of paracetamol in pregnancy and childhood asthma is unlikely to be confounded by unmeasured behavioural factors linked to paracetamol use. 


TIBITS—collected by JK from Wikipedia:   

Its diagnosis is usually made based on the pattern of symptoms and/or response to therapy over time.[10] The prevalence of asthma has increased significantly since the 1970s. As of 2010, 300 million people were affected worldwide.[11] In 2009 asthma caused 250,000 deaths globally.[  Some 9% of US children had asthma in 2001, compared with just 3.6% in 1980. One subject that appears to show a strong correlation is the development of asthma and obesity. In the United Kingdom and United States, the rise in asthma prevalence has echoed an almost epidemic rise in the prevalence of obesity.  In Taiwan, symptoms of allergies and airway hyper-reactivity increased in correlation with each 20% increase in body-mass index.[54]  Maternal tobacco smoking during pregnancy and after delivery is associated with a greater risk of asthma-like symptoms, wheezing, and respiratory infections during childhood.[64]  The strongest risk factor for developing asthma is a history of atopic disease;[37] {hyper allergenic people} this increases one's risk of hay fever by up to 5 and the risk of asthma by 3–4.[38]  Asthma prevalence in the US is higher than in most other countries in the world, but varies drastically between diverse US populations.[61] In the US, asthma prevalence is highest in Puerto Ricans, African Americans, Filipinos, Irish Americans, and Native Hawaiians, and lowest in Mexicans and Koreans.  During the 1930s–50s, asthma was considered as being one of the 'holy seven' psychosomatic illnesses. Its aetiology was considered to be psychological, with treatment often based on psychoanalysis and other 'talking cures'.[171] As these psychoanalysts interpreted the asthmatic wheeze as the suppressed cry of the child for its mother, so they considered that the treatment of depression was especially important for individuals with asthma.[171] among the first papers in modern medicine, is one that was published in 1873 and this paper tried to explain the pathophysiology of the disease.[172] Through the end of 2005, 25 genes had been associated with asthma in six or more separate populations:[84]  The genetic trait, CD14 single nucleotide polymorphism (SNP) C-159T and exposure to endotoxin (a bacterial product) are a well-replicated example of a gene-environment interaction that is associated with asthma. 


There is a significant association between asthma-like symptoms (wheezing) among preschool children and the concentration of DEHP (phthalates) in indoor environment.[79] DEHP (di-ethylhexyl phthalate) is a plasticizer that is commonly used in building material. The hydrolysis product of DEHP (di-ethylhexyl phthalate) is MEHP (Mono-ethylhexyl phthalate) which mimics the prostaglandins and thromboxanes in the airway leading to symptoms related to asthma.[80] Another mechanism that has been studied regarding phthalates causation of asthma is that high phthalates level can "modulate the murine immune response to a coallergen". Asthma can develop in the adults who come in contact with heated PVC fumes.[81] Two main type of phthalates, namely n-butyl benzyl phthalate (BBzP) and di(2-ethylhexyl) phthalate (DEHP), have been associated between the concentration of polyvinyl chloride (PVC) used as flooring and the dust concentrations. Water leakage were associated more with BBzP, and buildings construction were associated with high concentrations of DEHP.[82] Asthma has been shown to have a relationship with plaster wall materials and wall-to wall carpeting. The onset of asthma was also related to the floor–leveling plaster at home. Therefore, it is important to understand the health aspect of these materials in the indoor surfaces.[83]




The Lancet, Volume 372, Issue 9643, Pages 1039 - 1048, 20 September 2008 doi:10.1016/S0140-6736(08)61445-2



Exposure to paracetamol during intrauterine life, childhood, and adult life may increase the risk of developing asthma. We studied 6—7-year-old children from Phase Three of the International Study of Asthma and Allergies in Childhood (ISAAC) programme to investigate the association between paracetamol consumption and asthma.


As part of Phase Three of ISAAC, parents or guardians of children aged 6—7 years completed written questionnaires about symptoms of asthma, rhinoconjunctivitis, and eczema, and several risk factors, including the use of paracetamol for fever in the child's first year of life and the frequency of paracetamol use in the past 12 months. The primary outcome variable was the odds ratio (OR) of asthma symptoms in these children associated with the use of paracetamol for fever in the first year of life, as calculated by logistic regression.


205 487 children aged 6—7 years from 73 centres in 31 countries were included in the analysis. In the multivariate analyses, use of paracetamol for fever in the first year of life was associated with an increased risk of asthma symptoms when aged 6—7 years (OR 146 [95% CI 136—156]). Current use of paracetamol was associated with a dose-dependent increased risk of asthma symptoms (161 [146—177] and 323 [291—360] for medium and high use vs no use, respectively). Use of paracetamol was similarly associated with the risk of severe asthma symptoms, with population-attributable risks between 22% and 38%. Paracetamol use, both in the first year of life and in children aged 6—7 years, was also associated with an increased risk of symptoms of rhinoconjunctivitis and eczema.


Use of paracetamol in the first year of life and in later childhood, is associated with risk of asthma, rhinoconjunctivitis, and eczema at age 6 to 7 years. We suggest that exposure to paracetamol might be a risk factor for the development of asthma in childhood.


The BUPA Foundation, the Health Research Council of New Zealand, the Asthma and Respiratory Foundation of New Zealand, the Hawke's Bay Medical Research Foundation, the Waikato Medical Research Foundation, Glaxo Wellcome New Zealand, the New Zealand Lottery Board, Astra Zeneca New Zealand, and Glaxo Wellcome International Medical Affairs.



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