Effects of indoor pollutants on atopic diseases

PollutantsEffects on asthma, AR, and AD
PM

Asthma:

  • Modulation of cell signaling pathways (involving i.e., IL-1b, GM-CSF, CCL2/MCP-1, and CCL20/MIP-3) for the recruitment towards the pulmonary tissue of dendritic cells that internalize particles, with consequent induction of type 2 response, reduction of airway remodeling and increase of hyper-responsiveness [1417]

  • The positive association between:

    • Coarse PM level and days of cough, wheezing, or chest tightness [18]

    • PM2.5 level and days of severe wheezing [18]

    • PM2.5 level and days of rescue medication needed [18]

    • Indoor PM levels and occurrence, prevalence, and exacerbation of asthma [1721]

    • Indoor PM levels and decreased lung function (FEV1, FEV1/FVC ratio, and MMEF) [2224]

  • Increased FeNO in all patients highly exposed to residential wood burning, regardless of their asthma status [22]

  • Decreased expression of junction proteins and increased release of pro-inflammatory cytokines (i.e., TSLP) in nasal epithelial cells exposed to PM2.5 in vitro [25]

AR:

  • Positive association between long-term exposure to PM2.5 (outdoor) and the severity of symptoms [26]

  • No association with indoor exposure to PM10 at school [27]

AD:

  • PM2.5 and PM10 both affect AD, probably due to increased ROS-mediated damage in the stratum corneum [28]

  • The positive association between levels of PM and the number of visits for AD [29, 30]

VOCs

Asthma and AR:

  • Propylene glycol: dehydration of the respiratory mucus gel layer, overproduction of mucus (goblet cell metaplasia), thickening of the mucosa, decreased mucociliary clearance. Exacerbations of asthma, with coughing and wheezing [35]

  • Formaldehyde: increase in the risk of developing asthma in highly exposed, especially in the presence of runny nose and hayfever [36]

  • Ethylbenzene: most important cause of emergency room visits for asthma among VOCs [37]

  • Higher rates of asthma, exacerbations, respiratory symptoms (current wheeze, dyspnea, nocturnal cough, and rhinitis), and lower lung function (decrease of FEV1 percent predicted) in children living near a petrochemical plant (exposure to both PM and VOCs) [38]

  • The positive association between exposure during childhood to VOCs from cleaning products and recurrent wheezing with atopy and asthma diagnosis [39]

AD:

  • Irritant action: worsening of AD symptoms [41, 42]

  • Toluene: upregulation of TSLP expression [42]

  • Toluene and mandelic acid: a positive association between their urinary metabolites of and SCORAD positive results [41]

Heavy metals

Asthma:

  • Vanadium: short-term indoor exposure is related to alteration in DNA methylation of allergic and pro-inflammatory asthma genes (IL-4) in children, but not to decrements in lung function [43]

  • Nickel, cobalt, and chromium: positive association between their positivity to patch tests and a history of atopic eczema [44]

  • Lead: indoor levels < 0.5 µg/m3 may affect AD [45]

Chemical gases

Asthma and AR:

  • Discording evidence about the association between higher indoor (NO2) and asthma [20, 21, 47]

  • The positive association between higher (SO2) and incidences of asthma, bronchitis, and AR [48]

  • The positive association between high exposure to (O3) and prevalence of adult-onset asthma, wheezing, recurrent asthma symptoms, and higher (FeNO) in bleachery workers from pulp mills [50]

AD:

  • Positive correlation between higher (SO2) and (CO) and the number of visits for AD [30]

  • SO2: even a short time exposure (a few days) can be related to the exacerbation of AD, with a risk increase of 2.9% per 10 μg/m³ increment [51]

Molds

Asthma:

  • Molds are recognized and endocytosed by dendritic cells, which in turn activate Th2 and Th17 pathways. The fungal proteases can directly damage the lung epithelium resulting in the release of alarmins (IL-33, IL-25), which in turn stimulate Th2 and ILC2 [56]

  • The positive association between Aspergillus fumigatus exposure and a higher degree of broncho-obstruction. Discording evidence for Alternaria alternata, Penicillium spp., and Cladosporium spp. [54, 55]

  • The significant association between exposure to indoor mold with the prevalence of AD [57, 58]

AD: atopic dermatitis; AR: allergic rhinitis; CCL2: C-C motif ligand 2; CO: carbon monoxide; FeNO: fraction of exhaled nitric oxide; FEV1: forced expiratory volume in the first second; FVC: forced vital capacity; GM-CSF: granulocyte-macrophage colony-stimulating factor; ILC2: type 2 innate lymphoid cells; MCP-1: monocyte chemotactic protein-1; MIP-3: macrophage inflammatory protein-3; MMEF: maximal mid-expiratory flow; NO2: nitrogen dioxide; O3: ozone; PM: particulate matter; ROS: reactive oxygen species; SCORAD: scoring AD; SO2: sulfur dioxide; Th2: T helper 2; TSLP: thymic stromal lymphopoietin; VOCs: volatile organic compounds