A much smaller study also indicated that many VOCs are present at higher levels in homes than in offices . In the absence of exposure to environmental tobacco smoke , the geometric mean time-weighted micro-environment concentrations of many VOCs closely approximated measured personal concentrations of these compounds in subjects from Helsinki . Acceptable lifetime cancer risk benchmarks have been established for various VOCs. In a recent study that monitored VOC exposure of 25 adults in three districts in Minneapolis/St. Paul, only the 90th percentile of outdoor concentrations of benzene and carbon tetrachloride exceeded such benchmark concentrations . Conversely, even the median personal and residential indoor concentrations of benzene exceeded the benchmark, and the 90th percentile indoor and personal exposure levels were higher than the risk threshold for three of the other five VOCs for which benchmarks are available. Similarly, in the SHIELDS study of children from two inner-city schools in Minneapolis, researchers found that median indoor residential and personal exposure levels of p-dichlorobenzene and benzene were above the acceptable risk thresholds during at least one of the seasons of measurement . Other hazardous air pollutants listed in the Clean Air Act Amendment, such as styrene, benzaldehyde, phenol, 2-butoxyethanol, and hexanal,indoor cannabis grow system are mucous membrane irritants, although at far greater concentrations than are generally encountered in indoor environments. 2-Butoxyethanol and oxidation products of Dlimonene are skin-contact allergens .It was recently reported that formaldehyde at a concentration of 0.1 µg/mL increased the expression of intracellular adhesion molecule – 1 and vascular adhesion molecule-1 on human mucosal microvascular endothelial cells to an extent similar to the combination of interleukin -4 and tumor necrosis factor -α . It also promoted adhesion of eosinophils isolated from patients with allergic rhinitis to these cells.
No induction of adhesion molecules was observed with the VOCs; 1,2-, 1,3-, or 1,4- benzene; o-, m-, or p-xylene; or toluene at the same concentration. These observations might explain the finding of an increased number and proportion of eosinophils in nasal lavage fluid of healthy volunteers up to 18 h after exposure to 0.5 mg/m3 of formaldehyde for 2 h . In Swedish school personnel, formaldehyde concentrations were significantly associated with decreased nasal patency and increased levels of the inflammatory markers eosinophil cationic protein and lysozyme, but not myeloperoxidase, in nasal lavage . There are increasing indications that formaldehyde not only affects the upper respiratory tract but that it can also enhance allergic sensitization and, through this and possibly other mechanisms, can cause lower respiratory tract symptoms, including asthma. Formaldehyde has been shown to enhance sensitization in ovalbumin -immunized guinea pigs . Although chronic inhalation of formaldehyde does not appear to induce significant inflammation in the lower respiratory tract of non-sensitized mice or guinea pigs , it has been shown to increase the number of inflammatory cells in bronchoalveolar lavage fluid of OVA-immunized mice and to potentiate allergen-induced bronchoconstriction in OVA-immunized guinea pigs . Occupational or accidental exposure to formaldehyde occasionally has been associated with the development of asthma that can persist even after further exposure to formaldehyde is avoided . In some of these cases, specific inhalation challenges identified formaldehyde resin dust, but not gaseous formaldehyde, as the cause of asthma symptoms . Whereas formaldehyde gas is largely absorbed in the upper respiratory tract, formaldehyde in particulate form could reach the lower respiratory tract, which could explain its greater ability to cause airway responses. Because products made from urea–formaldehyde resins, such as particleboard and medium-density fiberboard, are used extensively in the construction of new houses, formaldehyde resin dust may also be in residential environments. Although wood products are the sources that emit the highest amounts of formaldehyde, a wide variety of other products also contribute to indoor formaldehyde pollution .
ETS is another important source of formaldehyde. Mean or median residential indoor formaldehyde concentrations of 15 to 30 µg/m3 have been reported in several recent studies from the United States and Australia . Maxima ranged between 139 and 408 µg/m3 , indicating that some homes largely exceed current indoor guidelines . Notably, with increasing awareness of the adverse health effects of formaldehyde, the guideline values have been steadily decreasing. Currently, the lowest guideline value is the chronic inhalation reference exposure level of 3 µg/m3 set by the Office of Environmental Health Hazard Assessment of the California EPA. Chronic relevance exposure levels are concentrations or doses at or below which adverse health effects are not likely to occur. Despite the relatively low concentrations of formaldehyde in homes compared with occupational exposure levels, chronic domestic or other indoor exposure to this chemical can result in sensitization to formaldehyde itself and can enhance the incidence and severity of atopic sensitization to common allergens . Importantly, residential formaldehyde exposure has been associated with inflammation of the lower respiratory tract as well as asthma and other lower respiratory tract symptoms in children and adults. Concentrations of exhaled nitric oxide , which is believed to represent a marker of pulmonary inflammation, were found to be significantly higher in healthy children age 6 to 13 yr who were exposed to residential concentrations of formaldehyde of 50 ppb or greater compared to those exposed to levels less than 50 ppb . The technique used in this study ensured that the exhaled NO originated from the lower respiratory tract. This suggests that formaldehyde exposure may have induced an inflammatory response, even in children without signs or symptoms of upper or lower respiratory tract disease. The prevalence of asthma and chronic bronchitis was significantly greater in children, but not adults, from homes with formaldehyde concentrations greater than or equal to 60 ppb compared with those exposed to lower levels . A linear decrease in peak expiratory flow rates was observed with increasing formaldehyde exposure. A study of Swedish adults found significantly higher levels of both VOCs and formaldehyde in connection with indoor painting within the last 12 mo, and, in turn, exposure to recently painted surfaces was associated with increased symptoms related to asthma and current asthma as well as at least one asthma-related symptom in adults .In young children who were discharged from the emergency department with asthma as the primary diagnosis, there was a significant association between case status and higher residential formaldehyde exposure compared with age-matched controls .
In the same group of children, a significant correlation was also detected between total and individual domestic VOC levels and asthma; benzene, ethylbenzene, and toluene were each associated with significantly increased ORs . Note that it is difficult to determine whether wheezing illness in such young children truly constitutes asthma. Total VOCs measured in 96 Japanese homes carried significantly elevated ORs for throat and respiratory symptoms in the 317 residents of these buildings . Xylene, α-pinene, and nonanal were the three individual VOCs significantly associated with these symptoms. An association between VOC exposure and asthma has further been suggested by the finding that urinary concentrations of muconic acid and 1-hydroxypyrene were elevated in children with asthma compared with children without wheezing episodes or atopic diseases . In partial contrast, in a study of 193 children with persistent wheezing illness and 223 controls age 9 to 11 yr, no association was detected between formaldehyde or individual or total VOCs and case status . However, the frequency of nocturnal symptoms was associated with formaldehyde exposure but not with VOC concentrations. In Swedish adults, cannabis grow equipment nocturnal breathlessness was significantly associated with both the formaldehyde and the VOC concentrations in their homes . Residential formaldehyde exposure was not significantly associated with the risk of asthma or respiratory symptoms in a group of 148 Australian children age 7 to 14 yr, although the maximum recorded formaldehyde values of four 4-d samples were associated with atopic sensitization . Note that this is one of the few studies in which exposure was measured on several occasions through the year. In most studies, only single measurements of formaldehyde and/or VOCs were taken. Therefore, in our opinion, the associations with allergic sensitization or asthma observed in such studies should be interpreted with considerable caution. The limited data available indicate that there are substantial day-to-day, daytime vs nighttime, and seasonal fluctuations in VOC exposure resulting not only from changes in the environment over time but also from differences in sources and activities that result in exposure . Intra-individual variation over multiple monitoring periods was found to span two orders of magnitude for each of the 14 VOCs measured in personal air . Additionally, residential indoor VOC concentrations are consistently lower than levels measured in the personal air space of both adults and children , indicating that they do not fully reflect personal exposure. Furthermore, it is not clear whether peak exposure or chronic low-level exposure constitutes a greater risk for atopy and asthma. Concentrations of indoor VOCs and formaldehyde generally exceed outdoor concentrations by as much as an order of magnitude . This clearly shows that they are emitted from indoor sources and are not transported in from the outside. Sources, rather than types and rate of ventilation, were associated with indoor formaldehyde, VOC, CO, and NO2 levels in homes . This was at least partly confirmed by a Finnish study of VOCs that combined personal exposure assessment with measurements in residential and work environments . ETS was found to be a dominant source of personal VOC exposure. In ETS-free homes, variability in VOC exposure stemmed from compounds associated with cleaning products, followed by compounds associated with traffic emissions, long-rangetransport of pollutants, and product emissions . Together, these data suggest that source control constitutes the most effective way of reducing environmental exposure to formaldehyde and VOCs.Phthalates are dialkyl- or alkylarylesters of 1,2-benzenedicarboxylic acid.
The major representative is di phthalate , of which the worldwide annual consumption exceeds two million tons . Waste that contains DEHP is estimated to emit another 100,000 tons of DEHP annually. Total worldwide phthalate consumption is estimated at 3.25 million tons. DEHP and other phthalates are used as plasticizers in polyvinyl chloride products, which may contain up to 40% DEHP. PVC resins are used to manufacture a wide variety of items, including floor tiles, vinyl upholstery, toys, disposable medical examination and surgical gloves, medical tubing, blood storage bags, components of paper, and paperboard. Additionally, phthalates are used as fixatives, detergents, lubrication oils, and solvents as well as in cosmetics and personal care products. Because phthalates are not covalently bound to PVC-based products, they leach and vaporize from plastic over time.The main exposure route is generally assumed to be ingestion, with fatty foods, such as dairy, fish, meat, and oils containing the highest levels, whereas inhalation and dermal contact make lesser contributions . However, in the case of diethyl phthalate used in personal care products, dermal absorption can probably substantially contribute to total exposure. Recently, the detection of several phthalate metabolites was reported in human breast milk, indicating that oral exposure can begin immediately after birth . Additionally, direct intravenous exposure occurs in patients undergoing dialysis or receiving blood transfusions. Note that there is limited evidence to support the hypothesis that food constitutes the major source of phthalates . Rather, a recent study found a significant correlation between the concentrations of di-n-butyl , butyl benzyl , and DEP in inhaled air and their urinary monoester metabolites . Correlation coefficients ranged from 0.65 for BBzP to 0.42 for DEP. Substantial amounts of various phthalates were also found to be adsorbed to suspended PM and may make even greater contributions to inhalation exposure than phthalates in the vapor phase . Together, these results suggest that inhalation may represent an important exposure route for at least some phthalates. Tables 4 and 5 summarize measurements of various phthalates in air and dust of residences, schools, and day care centers. The ubiquity of phthalates and the resulting high level of contamination of laboratory equipment made it difficult to assess the extent of exposure until measurement of monoester metabolites was introduced . After oral ingestion, phthalate diesters are hydrolyzed to their respective monoesters. The relatively polar and low-molecular-weight phthalates are excreted primarily as monoesters. The monoesters of phthalates with higher molecular weights, such as DEHP, di-n-octyl phthalate, and di-isononyl phthalate, undergo rather extensive ω-1 and ω-oxidation of their aliphatic sidechains . In humans, monoesters and the oxidative metabolites are excreted primarily as glucuronides .