***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Background : Allergic disease affects 30 % to 40 % of the world 's population , and its development is determined by the interplay between environmental and inherited factors . Air pollution , primarily consisting of diesel exhaust emissions , has increased at a similar rate to allergic disease . Exposure to diesel exhaust may play a role in the development and progression of allergic disease , in particular allergic respiratory disease . One potential mechanism underlying the connection between air pollution and increased allergic disease incidence is DNA methylation , an epigenetic process with the capacity to integrate gene‐environment interactions . Objective : We sought to investigate the effect of allergen and diesel exhaust exposure on bronchial epithelial DNA methylation . Methods : We performed a r and omized crossover‐controlled  exposure study to allergen and diesel exhaust in humans , and measured single‐site ( CpG ) resolution global DNA methylation in bronchial epithelial cells . Results : Exposure to allergen alone , diesel exhaust alone , or allergen and diesel exhaust together ( coexposure ) led to significant changes in 7 CpG sites at 48 hours . However , when the same lung was exposed to allergen and diesel exhaust but separated by approximately 4 weeks , significant changes in more than 500 sites were observed . Furthermore , sites of differential methylation differed depending on which exposure was experienced first . Functional analysis of differentially methylated CpG sites found genes involved in transcription factor activity , protein metabolism , cell adhesion , and vascular development , among others . Conclusions : These findings suggest that specific exposures can prime the lung for changes in DNA methylation induced by a subsequent insult Histone acetylation status is a key factor in the regulation of inflammatory gene transcription . We investigated the activity of histone acetylases ( HAT ) and deacetylases ( HDAC ) , and the effect of glucocorticoids in alveolar macrophages ( AM ) and peripheral blood mononuclear cells ( P BMC ) from subjects with asthma .  Bronchoalveolar lavage was performed in 10 patients with intermittent asthma , 8 with persistent asthma , and 10 healthy control subjects . P BMC s and granulocytes were isolated from six patients with mild and severe asthma , before and after a 7-day course of prednisolone ( 30 mg/day ) . AMs were isolated for HDAC assay or incubated with dexamethasone ( 1 microM ) . HAT activity was increased ( 1.43 + /- 0.1 vs. 1.01 + /- 0.1 st and ard units/10 microg , p < 0.05 ) , and HDAC activity was reduced ( 3031 + /- 243 vs. 5004 + /- 164 arbitrary fluorescence units/10 microg , p < 0.001 ) in AMs of subjects with asthma compared with control subjects . Dexamethasone suppressed LPS-induced granulocyte macrophage-colony stimulating factor , tumor necrosis factor-alpha , and interleukin-8 release by 83 + /- 1 % , 51 + /- 7 % and 20 + /- 9 % ( p < 0.001 ) , respectively . Similar effects were seen on nuclear factor-kappaB inhibition , and interleukin-8 release was further reduced by the HDAC enhancer , theophylline ( 37 + /- 6 % ) . Prednisolone increased HDAC activity in P BMC s from subjects with mild asthma . The increased inflammatory response in asthma may be due to reduced HDAC and enhanced HAT activity . Glucocorticoids and theophylline may downregulate the inflammatory response by modulating HAT and HDAC activity , and nuclear factor-kappaB activation BACKGROUND The natural history of allergic disease and its potential for prevention merit close examination because of the explosive worldwide increase in the prevalence and morbidity of atopic disorders . This study examines the development of atopy at age 7 years in 165 children in a high-risk cohort , previously reported from birth to age 4 years . METHODS In this prospect i ve , r and omized , controlled study of food allergen avoidance in infancy , the prophylactic-treated group consisted of infants whose mothers avoided cow 's milk , egg , and peanut during the last trimester of pregnancy and lactation and who , themselves ,  avoided cow 's milk until age 1 year ( casein hydrolysate supplementation before age 1 ) , egg until age 2 years , and peanut and fish until age 3 years . The control group consisted of maternal/infant pairs who followed st and ard feeding practice s. RESULTS Despite a significant reduction in food allergy and milk sensitization before age 2 years , none of the following differed between the groups at age 7 years : food allergy , atopic dermatitis , allergic rhinitis , asthma , any atopic disease , lung function , food or aeroallergen sensitization , serum IgE level , or presence of nasal eosinophils or nasal basophilic cells .  Children with food allergy by 4 years evidence d higher 7-year ( current ) prevalences of allergic rhinitis and asthma ( p < 0.01 ) . Atopic diseases/parameters at age 7 years were shown , by multivariate analysis ( p < 0.05 ) , to be associated with several genetic and environmental risk factors ( male gender , maternal nonwhite ethnicity and asthma , and household smoking ) , as well as predictive atopic markers during infancy ( elevated serum IgE level ; egg , cow 's milk , and peanut sensitization ; and nasal eosinophils and nasal basophilic cells ) . CONCLUSIONS These findings help to : ( 1 ) eluci date the natural history of atopic disease in high-risk children ; ( 2 ) document the progression of allergy from atopic dermatitis , food allergy , and food sensitization to respiratory allergy and aeroallergen sensitization despite food allergy prevention in infancy ; ( 3 ) identify allergy predictive markers ; and ( 4 ) exp and our appreciation of the interactions of genetic and environmental factors in the development of atopy 
    Output:
    
We found that environmental factors during early development are related to epigenetic effects that may be associated with a higher risk of CRDs .
Epigenetic dysregulation of gene expression of the histone deacetylase ( HDAC ) and histone acetyltransferase gene families was likely involved in lung health of slum dwellers .
Respiratory-related environmental exposures influence HDAC function and deoxyribonucleic acid methylation and are important risk factors in the development of CRD .