{"id":60127,"date":"2024-09-30T11:40:39","date_gmt":"2024-09-30T11:40:39","guid":{"rendered":"https:\/\/biomedpharmajournal.org\/?p=60127"},"modified":"2025-02-27T08:05:24","modified_gmt":"2025-02-27T08:05:24","slug":"phthalate-exposure-and-pediatric-asthma-a-case-control-study-among-egyptian-children","status":"publish","type":"post","link":"https:\/\/biomedpharmajournal.org\/staging\/vol17no3\/phthalate-exposure-and-pediatric-asthma-a-case-control-study-among-egyptian-children\/","title":{"rendered":"Phthalate Exposure and Pediatric Asthma: A Case Control Study Among Egyptian Children"},"content":{"rendered":"\n

Introduction<\/strong><\/p>\n\n\n\n

Bronchial\nasthma is a widespread chronic disease in childhood, affecting up to 20% of\nchildren worldwide with significant geographic variations in prevalence,\nseverity, and mortality 1<\/sup><\/sup>. According to\nWHO records, asthma affected more than 339 million people globally in 2016,\nresulting in a significant burden of the disease globally, with approximately\n10-15% of children affected.2<\/sup>.In Egypt, the\nprevalence of asthma ranges between 7.7-8.2% 3,4<\/sup>.  The international\nvariations of asthma burden are still unclear, although genetic predisposition\nis evident. Environmental factors such as infections and exposure to\nenvironmental endotoxins may act as risk factors 5<\/sup>.<\/p>\n\n\n\n

Suggested theory assumed that one potential risk factor for\nthe raising prevalence of atopic (IgE-mediated) allergic diseases especially\nasthma in different countries, is exposure to constituents as environmental\npollutants and plasticizers such as phthalates that act as adjuvants. Specified\nfrequently used phthalate plasticizers, such as di-(2-ethylhexyl) phthalate, was\nlinked to this regard 6<\/sup>. In Egypt, few studies investigated the exposure of\nphthalates in children and documented that plastic toys and bottled water are the\nmain sources of exposure 7-9<\/sup>.<\/p>\n\n\n\n

Phthalates are plasticizers, solvents, and additives that are\nadded to PVC (polyvinyl chloride) plastics and several personal care products.\nPhthalates are synthetic organic compounds that are phthalic acid diesters 10<\/sup>. More than 25 phthalates are used in commercial items, which\nraises the quality of the item they are incorporated in 11<\/sup>.<\/p>\n\n\n\n

Many commercial products may have phthalates in their consistency\nincluding: building supplies, medical devices, packages of food, makeup\nproducts, fragrances, children’s toys, shampoos, teethers, epoxy resins,\ndecorating paint, floorboards, hair sprays, soaps, nail polishes, and cleaners 10-12<\/sup>.<\/p>\n\n\n\n

The production of phthalates was increased yearly worldwide\nfrom 4.7000,000 metric tons in 2006 13<\/sup> up to ~8 million metric tons in 2015 14<\/sup> The estimated global market of phthalates in 2020 has reached\n10 billion dollars and are still widely used in plastic devices and products 15<\/sup>.<\/p>\n\n\n\n

Exposure to phthalates in humans begins principally from\neating, consumption, inhalation, and absorption through skin 16,17<\/sup>. Studies in humans have assessed serum phthalate 18<\/sup> and phthalate metabolites in human urine 19,20<\/sup>, semen 21,22<\/sup> and breast milk 23,24<\/sup>. <\/p>\n\n\n\n

Although it is assumed that exposure to phthalates may prompt\noxidative stress and provoke respiratory consequences, it is doubtful in what\nway phthalates worsen respiratory function and initiate airway inflammation in asthmatic\npatients  16<\/sup> .<\/p>\n\n\n\n

Recent studies demonstrated the association of urinary\nphthalates concentration and exacerbation of asthmatic children 15,25-27<\/sup>.<\/p>\n\n\n\n

This study aims to compare\nurinary phthalates concentrations in asthmatic children with those in a control\ngroup and to identify potential sources of phthalates exposure as risk factors\nfor asthma development.<\/p>\n\n\n\n

Methods<\/strong><\/p>\n\n\n\n

This study was held as a\ncase control study on children selected from those attending pulmonary clinic\nat Abo El Reesh Specialized Pediatric Hospital, Cairo University. Children aged\nbetween 8 and 16 years. Fifty children were selected at random out of asthmatic\nchildren with variable degrees of severity corresponding to (GINA) Guidelines 28<\/sup>. Fifty apparently healthy children were recruited from the relatives of patients of matched age\nand gender, who lived in another house and\/or environment through an\nannouncement.<\/p>\n\n\n\n

Ethical approval<\/strong><\/p>\n\n\n\n

“Ethical\napproval was obtained from the Medical Ethics Committee of the National\nResearch Centre, Egypt (approval number 16-368). Written informed consent was\nobtained from all parents or legal guardians of the participating children. The\nstudy adhered to the International Ethical<\/p>\n\n\n\n

Guidelines\nfor Biomedical Research Involving Human Subjects 29<\/sup> . <\/p>\n\n\n\n

Inclusion criteria and Exclusion criteria<\/strong><\/p>\n\n\n\n

Children diagnosed with asthma, either in remission or during\nan acute attack, based on clinical presentation. Exclusion criteria: Children\nwith a history of renal, liver, thyroid, or endocrine diseases were excluded\nfrom both the case and control groups.”<\/p>\n\n\n\n

Data collection and clinical examination<\/strong><\/p>\n\n\n\n

Data collection involved administering a questionnaire to the\nchildren and their guardians, covering socio- demographic variables and\npotential risk factors such as the age of the residential building, indoor environmental\nexposure (e.g., plastic\/vinyl flooring, type of home painting), exposure to\npassive smoking, and the frequent use of personal care products (e.g., shampoo,\nhair gel\/spray, lotions, toothpaste, perfumes). Both groups underwent a general\nand chest clinical examination. Asthma was assessed using the GINA 2019\nguidelines, and chest radiographs were reviewed for the asthmatic group to\nverify the diagnosis. Early morning urine samples were collected from both\nasthmatic and control children and stored at -70\u00b0C until analysis.”<\/p>\n\n\n\n

Laboratory investigations<\/strong><\/p>\n\n\n\n

Urinary phthalates were the definite biomarkers of phthalate exposure\nin previous studies 30,31<\/sup> As phthalates are metabolized to their mono-esters in few\nhours or maximum days. Urinary phthalate mono-esters are valuable biomarkers\nfor evaluating human phthalate exposure 32<\/sup>. One spot urine sample is adequately expressive for six\nmonths exposure 33<\/sup>. <\/p>\n\n\n\n

Urinary creatinine was included as a covariate in all\nanalyses as to correct dilution,  We adjusted all metabolite\nconcentrations  for creatinine levels and\nwas expressed as \u03bcg\/g Cr.<\/p>\n\n\n\n

Urine samples were thawed and sonicated for 10\u201315 min, then\n(100 \u03bcl) was loaded into a glass vial (2 ml) containing ammonium acetate (AA,\n20 \u03bcl, >98%, Sigma Aldrich Laboratory, Inc., St. Louis, MO, USA),\n\u03b2-glucuronidase (10 \u03bcl, E.coli K12, Roche Biomedical, Mannheim, Germany), and a\ncombination of ten isotopic 13C4) phthalate metabolite standards (100 \u03bcl.\nCambridge Isotope Laboratory, Inc., Andover, MA, USA). Afterward, the samples\nwere incubated (37\u2103, 90 min), a 270 \u03bcl solution (5% ACN), Merck, Darmstadt,\nGermany) with 0.1% formic acid (FA, Merck, Darmstadt, Germany) was added and\nsealed with the PTEF cap for analysis. Monoethyl phthalate, monomethyl\nphthalate, monobenzyl phthalate, monobutyl phthalate, and\nbis2ethylhexylphthalate were purchased from SigmaAldrich. \u03b2-glucuronidase was\npurchased from Roche. Stock solutions of standards were prepared in\nacetonitrile (3000ng\/ml). Eleven-point calibration curve was constructed for\neach standard (0.5, 1, 2, 4, 8, 16, 32, 64, 128, 256, and 1000 ng\/ml). Sample\npreparation was done by solid-phase extraction according to the method\ndescribed 28<\/sup> After evaporation of eluting, the residue was reconstituted\nin 100 \u00b5l 20% acetonitrile in water and injected.<\/p>\n\n\n\n

Phthalate metabolites were assessed as an alternative of\ntheir parent compounds to lower the potential for exposure misclassification. A\ncombination of solid phase extraction, high pressure liquid chromatography, and\ntandem mass spectrometry were used to measure phthalate metabolite levels using\nmethods described by a group of researches 34<\/sup> .<\/p>\n\n\n\n

Statistical analysis<\/strong><\/p>\n\n\n\n

Statistical analyses were performed using the Statistical\nPackage for Social Sciences (SPSS) version 21 (IBM Corp., Armonk, NY, USA).\nContinuous variables were presented as mean \u00b1 standard deviation and compared\nusing the student\u2019s t- test. Categorical variables were presented as\nfrequencies and percentages and analyzed using the two-tailed chi-square test.\nOdds ratios (OR), 95% confidence\nintervals (CI), and logistic regression analyses were conducted to identify\npotential risk factors and predictors of bronchial asthma. A p-value of\n<0.05 was considered statistically significant.<\/p>\n\n\n\n

Results<\/strong><\/p>\n\n\n\n

Table 1 presents the descriptive data of the studied groups. The mean age of the asthmatic group was 11.78 \u00b1 1.28 years, and the control group was 12.35 \u00b1 1.44 years, with no significant difference between the groups. The gender distribution was similar, with 56% females and 44% males in the asthmatic group, and 60% females and 40% males in the control group, showing no significant difference. \u201cThe children with asthma had higher concentrations of some urinary phthalate metabolites than the control group. Mean Mono-methyl and Mono-benzyl levels were significantly higher in asthmatic children (895.26 ng\/mL and 13.5 ng\/mL) compared to the control group (548.55 ng\/mL and 2.07 ng\/mL, respectively; p=0.001) The mean urinary levels of the other two studied phthalate metabolites (Mono 2ethylhexyl and Mono-butyl phthalate) showed insignificant difference (p>0.05).<\/p>\n\n\n\n

Table 1: Urinary phthalate metabolites level between asthmatics versus control groups<\/strong><\/p>\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n
\n

 <\/strong><\/p>\n<\/td>\n

\n

Groups<\/strong><\/p>\n<\/td>\n

\n

Mean \u00b1 SD<\/strong><\/p>\n<\/td>\n

\n

p–<\/em>value<\/strong><\/p>\n<\/td>\n<\/tr>\n

\n

 Ag<\/p>\n<\/td>\n

\n

Bronchial asthma<\/p>\n<\/td>\n

\n

11.78\u00b1 1.28<\/p>\n<\/td>\n

\n

0.132<\/p>\n<\/td>\n<\/tr>\n

\n

control<\/p>\n<\/td>\n

\n

12.35\u00b1 1.44<\/p>\n<\/td>\n<\/tr>\n

\n

Mono (2ethylhexyl) phthalate (MEHP) (ng\/ml)<\/p>\n<\/td>\n

\n

Bronchial asthma<\/p>\n<\/td>\n

\n

61.50\u00b1 9.77<\/p>\n<\/td>\n

\n

0.965<\/p>\n<\/td>\n<\/tr>\n

\n

control<\/p>\n<\/td>\n

\n

60.56 \u00b1 24.72<\/p>\n<\/td>\n<\/tr>\n

\n

Mono-methyl phthalate<\/p>\n

(ng\/ml)<\/p>\n<\/td>\n

\n

Bronchial asthma<\/p>\n<\/td>\n

\n

895.26\u00b1102.68<\/p>\n<\/td>\n

\n

0.001*<\/p>\n<\/td>\n<\/tr>\n

\n

control<\/p>\n<\/td>\n

\n

548.55\u00b146.97<\/p>\n<\/td>\n<\/tr>\n

\n

Mono-benzyl phthalate<\/p>\n

(ng\/ml)<\/p>\n<\/td>\n

\n

Bronchial asthma<\/p>\n<\/td>\n

\n

13.50\u00b117.09<\/p>\n<\/td>\n

\n

0.001*<\/p>\n<\/td>\n<\/tr>\n

\n

control<\/p>\n<\/td>\n

\n

2.07 \u00b1 0.96<\/p>\n<\/td>\n<\/tr>\n

\n

Mono-butyl phthalate<\/p>\n

(ng\/ml)<\/p>\n<\/td>\n

\n

Bronchial asthma<\/p>\n<\/td>\n

\n

28.59\u00b1 9.38<\/p>\n<\/td>\n

\n

0.089<\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

*p < 0.05 is significant.<\/p>\n\n\n

The association between asthma and potential sources of exposure was reported in table (2), where the number of asthmatic children living in houses painted with non-plastic paint was significantly lower (P=0.001) than children living in houses painted with plastic paints. The presented results showed that, the subjects exposed to passive smoking were significantly more likely to have bronchial asthma compared to those not exposed to passive smoking (p=0.001). Moreover, the subjects who frequently used personal care products were significantly more at risk of having bronchial asthma compared to those not frequently used these products (p =0.001). On the other hand, “Table 2 shows the association between asthma and potential sources of exposure. A significantly lower number of asthmatic children lived in houses painted with non-plastic paint compared to plastic paints (p = 0.001). Exposure to passive smoking was significantly associated with a higher likelihood of bronchial asthma (p = 0.001). Additionally, frequent use of personal care products significantly increased the risk of asthma (p = 0.001). However, the age of the residential building showed no association with the risk of developing asthma.”<\/p>\n\n\n\n

Table 2: Exposure to potential sources of phthalate in asthmatic versus control groups<\/strong><\/p>\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n
\n

\u00a0<\/strong><\/p>\n<\/td>\n

\n

\u00a0<\/p>\n<\/td>\n

\n

OR<\/p>\n<\/td>\n

\n

95% CI<\/p>\n<\/td>\n

\n

P-value<\/p>\n<\/td>\n<\/tr>\n

\n

Bronchial asthma<\/p>\n<\/td>\n

\n

control<\/p>\n<\/td>\n<\/tr>\n

\n

Age of house building<\/p>\n<\/td>\n

\n

\u2264 10<\/p>\n

years<\/p>\n

\u00a0<\/strong><\/p>\n<\/td>\n

\n

Count<\/p>\n<\/td>\n

\n

10<\/p>\n<\/td>\n

\n

10<\/p>\n<\/td>\n

\n

1.053<\/p>\n<\/td>\n

\n

0.394-2.812<\/p>\n<\/td>\n

\n

0.919<\/p>\n<\/td>\n<\/tr>\n

\n

% Within age of house building<\/p>\n<\/td>\n

\n

50.0%<\/p>\n<\/td>\n

\n

50.0%<\/p>\n<\/td>\n<\/tr>\n

\n

> 10<\/p>\n

years<\/p>\n<\/td>\n

\n

Count<\/p>\n<\/td>\n

\n

38<\/p>\n<\/td>\n

\n

40<\/p>\n<\/td>\n<\/tr>\n

\n

% Within age of house building<\/p>\n<\/td>\n

\n

48.7%<\/p>\n<\/td>\n

\n

51.3%<\/p>\n<\/td>\n<\/tr>\n

\n

Painting of the wall<\/p>\n

\u00a0<\/strong><\/p>\n<\/td>\n

\n

Non-plastic painting<\/p>\n

\u00a0<\/strong><\/p>\n<\/td>\n

\n

Count<\/p>\n<\/td>\n

\n

14<\/p>\n<\/td>\n

\n

34<\/p>\n<\/td>\n

\n

0.183<\/p>\n<\/td>\n

\n

0.078-0.431<\/p>\n<\/td>\n

\n

0.001*<\/p>\n<\/td>\n<\/tr>\n

\n

% within Painting of the wall<\/p>\n<\/td>\n

\n

29.2%<\/p>\n<\/td>\n

\n

70.8%<\/p>\n<\/td>\n<\/tr>\n

\n

Plastic painting<\/p>\n

\u00a0<\/strong><\/p>\n<\/td>\n

\n

Count<\/p>\n<\/td>\n

\n

36<\/p>\n<\/td>\n

\n

16<\/p>\n<\/td>\n<\/tr>\n

\n

% within Painting of the wall<\/p>\n<\/td>\n

\n

69.2%<\/p>\n<\/td>\n

\n

30.8%<\/p>\n<\/td>\n<\/tr>\n

\n

Exposure to passive smoking<\/p>\n

\u00a0<\/strong><\/p>\n<\/td>\n

\n

yes<\/p>\n

\u00a0<\/strong><\/p>\n<\/td>\n

\n

Count<\/p>\n<\/td>\n

\n

40<\/p>\n<\/td>\n

\n

23<\/p>\n<\/td>\n

\n

\u00a0<\/p>\n

\u00a0<\/p>\n

\u00a0<\/p>\n

\u00a0<\/p>\n

4.696<\/p>\n<\/td>\n

\n

`1.931-11.418<\/p>\n<\/td>\n

\n

0.001*<\/p>\n<\/td>\n<\/tr>\n

\n

% within Exposure to passive smoking<\/p>\n<\/td>\n

\n

63.5%<\/p>\n<\/td>\n

\n

36.5%<\/p>\n<\/td>\n<\/tr>\n

\n

No<\/p>\n

\u00a0<\/strong><\/p>\n<\/td>\n

\n

Count<\/p>\n<\/td>\n

\n

10<\/p>\n<\/td>\n

\n

27<\/p>\n<\/td>\n<\/tr>\n

\n

% within Exposure to passive smoking<\/p>\n<\/td>\n

\n

27.0%<\/p>\n<\/td>\n

\n

73.0%<\/p>\n<\/td>\n<\/tr>\n

\n

Frequent use of personal care products<\/p>\n

(more than once \/ week)<\/strong><\/p>\n<\/td>\n

\n

yes<\/p>\n

\u00a0<\/strong><\/p>\n<\/td>\n

\n

Count<\/p>\n<\/td>\n

\n

31<\/p>\n<\/td>\n

\n

5<\/p>\n<\/td>\n

\n

14.358<\/p>\n<\/td>\n

\n

4.842-42.579<\/p>\n<\/td>\n

\n

0.001*<\/p>\n<\/td>\n<\/tr>\n

\n

% within use of personal care products<\/p>\n<\/td>\n

\n

86.1%<\/p>\n<\/td>\n

\n

13.9%<\/p>\n<\/td>\n<\/tr>\n

\n

No<\/p>\n

\u00a0<\/strong><\/p>\n<\/td>\n

\n

Count<\/p>\n<\/td>\n

\n

19<\/p>\n<\/td>\n

\n

44<\/p>\n<\/td>\n<\/tr>\n

\n

% within use of personal care products<\/p>\n<\/td>\n

\n

30.2%<\/p>\n<\/td>\n

\n

69.8%<\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

*p < 0.05 is significant, Odds ratio (OR)<\/p>\n\n\n

Table (3) indicates no significant association between floor type and the risk of asthma, with statistically insignificant differences in the distribution of asthmatic and control subjects across different floor types (vinyl, plastic, or ceramic) (p > 0.05).<\/p>\n\n\n\n

Table 3: Association between floor type and asthma<\/strong> using Chi-square test<\/strong>.<\/p>\n\n\n\n\n\n\n\n\n\n\n\n\n
\n

 <\/p>\n<\/td>\n

\n

Group<\/strong><\/p>\n<\/td>\n

\n

X2<\/sup><\/strong><\/p>\n<\/td>\n

\n

p-value<\/strong><\/p>\n<\/td>\n<\/tr>\n

\n

Bronchial asthma<\/strong><\/p>\n<\/td>\n

\n

control<\/strong><\/p>\n<\/td>\n<\/tr>\n

\n

Floor type<\/p>\n<\/td>\n

\n

Plastic<\/p>\n<\/td>\n

\n

Count<\/p>\n<\/td>\n

\n

2<\/p>\n<\/td>\n

\n

0<\/p>\n<\/td>\n

\n

 <\/p>\n

4.000<\/p>\n<\/td>\n

\n

 <\/p>\n

0.135<\/p>\n<\/td>\n<\/tr>\n

\n

 <\/p>\n

% within Floor type<\/p>\n<\/td>\n

\n

100.0%<\/p>\n<\/td>\n

\n

0.0%<\/p>\n<\/td>\n<\/tr>\n

\n

Vinyl<\/p>\n<\/td>\n

\n

Count<\/p>\n<\/td>\n

\n

0<\/p>\n<\/td>\n

\n

2<\/p>\n<\/td>\n<\/tr>\n

\n

% within Floor type<\/p>\n<\/td>\n

\n

0.0%<\/p>\n<\/td>\n

\n

100.0%<\/p>\n<\/td>\n<\/tr>\n

\n

Others as ceramic<\/p>\n<\/td>\n

\n

Count<\/p>\n<\/td>\n

\n

48<\/p>\n<\/td>\n

\n

48<\/p>\n<\/td>\n<\/tr>\n

\n

% within Floor type<\/p>\n<\/td>\n

\n

50.0%<\/p>\n<\/td>\n

\n

50.0%<\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

P–<\/em>value is insignificant(p> 0.05)<\/p>\n\n\n

Multiple logistic regression analysis (Table 4) showed that the age of the house, passive smoking, and floor type were not statistically significant predictors of bronchial asthma. However, plastic wall painting and frequent use of personal care products were highly significant predictors of asthma (p = 0.001). Specifically, plastic wall painting (target 1, non-plastic paint 0) was identified as a significant risk factor for bronchial asthma (p = 0.001). In contrast, the absence of frequent use of personal care products (target 1, frequent use 0) was found to be protective against bronchial asthma (B =-2.684, p = 0.001).<\/p>\n\n\n\n

Table 4: Bronchial asthma Risk factors in the studied groups by multiple logistic regression analysis <\/strong><\/p>\n\n\n\n\n\n\n\n\n\n\n\n
\n

\u00a0<\/p>\n<\/td>\n

\n

B<\/strong><\/p>\n<\/td>\n

\n

S.E.<\/strong><\/p>\n<\/td>\n

\n

p-value<\/strong><\/p>\n<\/td>\n

\n

OR<\/strong><\/p>\n<\/td>\n

\n

95% CI<\/strong><\/p>\n<\/td>\n<\/tr>\n

\n

Age of housebuilding\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0<\/p>\n

\u00a0(\u2264 10 years vs> 10 years)<\/p>\n<\/td>\n

\n

-0.075<\/p>\n<\/td>\n

\n

0.626<\/p>\n<\/td>\n

\n

0.904<\/p>\n<\/td>\n

\n

0.927<\/p>\n<\/td>\n

\n

0.272- 3.166<\/p>\n<\/td>\n<\/tr>\n

\n

Floor type (plastic and vinyl vs others)<\/p>\n<\/td>\n

\n

-0.913<\/p>\n<\/td>\n

\n

0.862<\/p>\n<\/td>\n

\n

0.290<\/p>\n<\/td>\n

\n

0.401<\/p>\n<\/td>\n

\n

0.074- 2.174<\/p>\n<\/td>\n<\/tr>\n

\n

Wall Painting
(Non-plastic vs others)<\/p>\n<\/td>\n

\n

2.233<\/p>\n<\/td>\n

\n

0.618<\/p>\n<\/td>\n

\n

0.001*<\/p>\n<\/td>\n

\n

9.327<\/p>\n<\/td>\n

\n

2.780- 31.291<\/p>\n<\/td>\n<\/tr>\n

\n

Passive smoking exposure<\/p>\n

\u00a0(Yes vs no)<\/p>\n<\/td>\n

\n

-0.837<\/p>\n<\/td>\n

\n

0.628<\/p>\n<\/td>\n

\n

0.183<\/p>\n<\/td>\n

\n

0.433<\/p>\n<\/td>\n

\n

0.126- 1.484<\/p>\n<\/td>\n<\/tr>\n

\n

Use of personal care products\u00a0\u00a0\u00a0\u00a0 (yes vs no)<\/p>\n<\/td>\n

\n

-2.684<\/p>\n<\/td>\n

\n

0.698<\/p>\n<\/td>\n

\n

0.001*<\/p>\n<\/td>\n

\n

0.068<\/p>\n<\/td>\n

\n

0.017- 0.268<\/p>\n<\/td>\n<\/tr>\n

\n

Constant<\/p>\n<\/td>\n

\n

4.956<\/p>\n<\/td>\n

\n

3.246<\/p>\n<\/td>\n

\n

0.127<\/p>\n<\/td>\n

\n

142.022<\/p>\n<\/td>\n

\n

\u00a0<\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

B: Standard Coefficient*p < 0.05 is significant.<\/p>\n\n\n

Discussion<\/strong><\/p>\n\n\n\n

The present study documented\na significant association between urinary phthalate levels and asthma in\nchildren, as significantly higher concentrations\nof Mono-methyl and Mono-benzyl\nphthalate metabolites were reported in the asthmatic children than the control\ngroup. It is known that one potential\ncontributor in aggravating atopic allergic diseases and asthma in children is\nexposure to substances that could affect as adjuvants. Phthalate plasticizers,\nsuch as Mono-methyl and Mono- benzyl phthalates, have been implicated in the\ndevelopment of asthma.  Many recent\nresearch studied the effect of phthalate exposure and development of asthma but\nthe exposure mechanism and potential risk factors are still unclear 35-38<\/sup>.<\/p>\n\n\n\n

Phthalate\nplasticizers, such as Mono-methyl and Mono-benzyl phthalate, have been\nimplicated in the exacerbation of asthma. These substances can act as\nadjuvants, aggravating atopic allergic diseases and asthma. The lack of\ncovalent binding in some phthalate compounds leads to greater environmental\nexposure as they leach into the air, food, drinks, and personal care products.\nThese compounds enter the human body through ingestion, inhalation, and skin\nabsorption 39<\/sup>.<\/p>\n\n\n\n

Our results showed that the\nmetabolites of phthalates were higher in asthmatic children which supports the\ntheory that phthalate exposure may lead to or aggravate asthma. It is unclear\nhow phthalates aggravate airway inflammation in asthmatic patients. Regular\nexposure to phthalates may aggravate the risk of asthma or could extend its course\nby peroxisome proliferator activated receptors which facilitate anti-inflammatory\nprocess in the respiratory system and immune modulation 40<\/sup>. Also, increase in the proliferation of the bronchial lung\nmuscle cells could cause airway remodeling 41<\/sup> as well as in pro-inflammatory IL-6 and IL-8  production in the air way\nepithelial cells 42<\/sup> which work as adjuvants by promoting macrophage production\nof  inflammatory cytokines and chemokines\n43<\/sup>.Moreover, Phthalate exposure induces oxidative stress that worsens\nrespiratory outcomes. Asthma acute attacks were linked to increased oxidative\nstress 37, 39, 40 <\/sup>These results are in agreement with recent studies which\ndocumented high phthalate exposure in specific asthma subgroups, emphasizing\nits complex relationship with asthma44,45<\/sup>.  <\/p>\n\n\n\n

Another research documented that phthalate-induced\nenhancements of mast cell degranulation and eosinophilic infiltration, which are\nimportant aspects of the early inflammation phase and  especially in indoor dust in the homes of\nasthmatic children compared to non-asthmatic controls, indicating an\nassociation between concentrations of phthalates in indoor dust and wheezing\namong preschool children46<\/sup>. In recent pediatric animal module study, the authors provided\nevidence that high-dose probiotics supplementation might play a modulating role\nin diethylhexyl phthalate causes of allergic asthma47<\/sup> .<\/p>\n\n\n\n

Passive smoking is a well-known risk factor for childhood\nasthma. Tobacco smoke exposure, both direct and second-hand, significantly\ncontributes to asthma pathogenesis in children 48<\/sup> ; tobacco smoking\nand exposure to negative smoking are widely acknowledged to be causative\nfactors for asthma in children 49<\/sup>.The current study\ninvestigated the passive smoking as a potential source of phthalates in\nasthmatic children and this is in agreement with studies that reported\nassociation between urinary phthalates in smoking mothers and health hazards .This\nwas explained by the effect of oxidative stress caused by smoking, as a source\nof phthalates, on childhood asthma  50,51<\/sup><\/p>\n\n\n\n

Whether allergic reaction\ntowards phthalates occurs due to prenatal maternal exposure, or due to\npost-natal infant exposure is still controversial.  J\u00f8hnk and\nhis colleagues <\/em>52<\/sup> demonstrated that maternal exposure to phthalates was related\nto development of asthma by the first  5\nyears of life. In addition, Ku and Co-others  53<\/sup> suggested that early postnatal exposure has the higher risk 53<\/sup>. Moreover, a follow up study that investigated the phthalate\nexposure in both pre and post-natal period, proved that early phthalates exposure\nis linked to allergic sensitization and play a role in asthma development in the early\nyears of childhood 53<\/sup>.<\/p>\n\n\n\n

In the current research urinary phthalate was used as an\nindicator of exposure. It is well known that a one spot of urine is appropriately expressive\nof exposure throughout a six months period and justify its use for assessment\nin epidemiologic studies 54<\/sup> .<\/p>\n\n\n\n

In the present study, we assessed the regular exposure to products containing phthalates, and results showed that the more frequent use of personal care products was a significant predictor of asthma.55,56<\/sup>.<\/p>\n\n\n\n

In addition, living in homes with plastic painting of walls appeared as\na significant risk factor for developing bronchial asthma57<\/sup>, while those living in houses with non-plastic paint, were\nless likely to be asthmatics. Non-plastic painting of the wall of\nhouses might be protective against bronchial asthma58<\/sup>. Moreover, Our findings supported the theory that phthalates\nexposure has a role in enhancing the immune system response59<\/sup>.<\/p>\n\n\n\n

Limitation of the study<\/strong><\/p>\n\n\n\n

The results of this study cannot be generalized due to the\nsmall sample size. Additionally, the study did not account for children’s\nexposures in school settings, where they spend 6-8 hours daily 60<\/sup>. Also, the\nquestionnaire lacked detailed inquiry about early childhood exposures, which\nare critical as the early years of life are essential for the maturation of the\nimmune and respiratory systems. Child behavior plays a significant role in the\nrisk of exposure, as infants and toddlers who crawl on dust floors or come into\ndirect contact with floors or house painting are more prone to developing\nasthma. Further research should\nfocus on assessing exposure in school environments and raising awareness among\nyoung mothers about the risks of phthalate exposure.<\/p>\n\n\n\n

Conclusion<\/strong><\/p>\n\n\n\n

Our study found higher urinary phthalate levels in children with asthma. Moreover Plastic wall paint and frequent use of personal care products were identified as the principal predictors of asthma. With a molecular structure like hormones, phthalates have the potential to disrupt the immune and endocrine system, leading to health concerns regarding their detrimental impacts on development. It is important to note that children are particularly vulnerable and sensitive to phthalates, particularly during the early stages of growth and development.<\/p>\n\n\n\n

Acknowledgment<\/strong><\/p>\n\n\n\n

The author acknowledge the National Research Centre for supporting this work. <\/p>\n\n\n\n

Conflict of Interest<\/strong><\/p>\n\n\n\n

The authors declare no conflict of interest.<\/p>\n\n\n\n

Funding source<\/strong><\/p>\n\n\n\n

The research is\nfunded by National Research Centre: grant no.(11010147)<\/p>\n\n\n\n

References<\/strong><\/p>\n\n\n\n

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