The exposed and control groups were matched for demographic and anthropometric measurements e.g age (in years), level of education, weight (kgm), height (cm), and body mass index (BMI), they didn't show any statistically significant difference (P>0.05, Table 1).
This study revealed a significantly higher prevalence of health effects in adolescent females environmentally exposed to pesticides compared to the control group. Exposed participants had lower. AChE activity levels, impaired ventilatory functions and more prevalent respiratory manifestations.
The exposed adolescent females reported a significantly higher prevalence of respiratory manifestations as cough, wheezes, dyspnea, asthma (24%, 27 %,26% and 7%; respectively) compared to the control participants (10%, 6%, 4%, 6% and 0%; respectively) and also in post exposure than pre exposure season (P<0.05, Table 2, Figs. 2-3). Moreover, exposed adolescent females positive for these manifestations had significantly lower AChE levels than negative ones (P<0.05, Table 3).. These findings coincide with those of previous studies conducted on agricultural workers and pesticide applicators (Ohayo-Mitoko, 2000). Also, pesticide use in the kitchen or dining rooms was associated with an increased prevalence of wheezes among children under 18 years of age in the United States (Hoppin et al., 2002). A study on Canadian farmers reported a significant risk for asthma with use of carbamate insecticides (OR=1.8; 95% CI 1.1 - 3.1) compared to non-asthmatic farmers (Senthilselvan et al. 1992). This is further evidenced by lung dysfunction indicated by lower pulmonary function values as observed in asthmatic farmers exposed to. carbofuran, methomyl, and carbaryl pesticides (Mamane et al. 2015).
Additionally, the exposed adolescent females showed statistically significant lower spirometric measurements than the control ones. It was found that mean values of spirometric measurements as (FEV1%, FEV1/FVC%, FEF25-75% and PEF %) were significantly lower in the exposed group (99.14±17.59, 96.73±25.88, 91.17±23.96 and 55.07±18.23; respectively) than their controls (104.18±11.54, 103.81±13.09, 104.17±19.72 and 62.05±16.95; respectively) (P<0.05, Table 4). These findings are consistent with previous studies of spirometry and OP exposure in adults as Callahan et al. (2014) who found significantly lower FEV1% and FVC% among applicators compared to non-applicators. Also, these findings are supported by the results of Peiris-John et al. (2005) who found that lowered FVC% and OP exposure were associated in 25 occupationally exposed Sri Lankan farmers and 22 fishermen who lived within a 25 km radius of fields where OPs were sprayed than non-exposed controls. Similarly, Zhu et al. (2015) found that pesticide applicators aged from 15-24 years had lower spirometric measurements than non-applicators with the same age. However, among 89 greenhouse workers and 25 non-spraying controls in Spain spirometric measurements and exposure to OPs were not associated; OPs exposure was defined as a depression of more than 25% in plasma cholinesterase or 15% depression in AChE levels (Hernandez et al. 2008).
The association berween increased prevalence of respiratory symptms and the decreased measurenents could due to direct allergic effects from inhalation of OPs compounds or from the nicotinic effect of ACh due to inhibition of AChE.
This study showed statistically significant lower means of AChE level, total protein, albumin, albumin∕globulin (A∕G) ratio in the exposed at post exposure (238.49±23.83 IU/L, 6.74 ±1.13 gm∕l, 3.59±0.55 gm∕l and 1.61 ± 0.04; respectively) than either the controls (302.70±36.54 IU∕ L, 7.37±1.51 gm∕l, 4.07±o.53 gm∕l and 2.29±0.89; respectively) or the exposed at pre exposure season (299.60±42.87 IU∕L, 7.09±1.03 gm∕l, 3.94±0.59 gm∕l and 2.16±0.41; respectively (P<0.05, Fig. 1, Table 5).
On the other hand, statistically significant higher means of SGPT, SGOT, ALP, globulin, urea, and creatinine were found in the exposed group post season (24.65±3.72 u/l, 28.22±5.43 u/l, 169.11±49.33 u/l, 1.99±0.51gm/l, 28.27±4.72 mg/dl, and 1.02±0.08 mg/dl; respectively) than either of the controls (20.61±7.07 u/l, 25.61±6.73 u/l, 154.71±55.92 u/l, 1.68±0.59gm/l, 24.40±5.25 mg/dl, and 0.95±0.23 mg/dl; respectively) or the exposed in the pre exposure season (22.51±3.29 u∕l,, 26.06±4.12 u∕l, 169.11±48.33 u∕l, 1.93±0.50 gm∕l, 24.95±5.78 mg∕dl and 0.84±0.12 mg∕dl; respectively) (P<0.05, Table 5).
The statistically significant increase in SGOT and SGPT for the studied adolescent females agrees with other several studies that reported the deterioration of liver enzymes in association with exposure to pesticides (Farahat et al., 2003; Jørs et al., 2006 and Mansour and Mossa, 2009). Also, these results are in agreement with (El-Sobky et al., 1994) who found that there was a statistically significant increase in SGOT (≤ 42 vs. > 42 U/L) and SGPT (≤ 60 vs. > 60 U/L) at the end of cotton ginning season (1991-1992) (31% and 30%; respectively) for exposed 100 participants compared to 50 controls (12% and 12%; respectively).
Also, SGPT, SGOT, ALP, total plasma proteins, albumin, globulin, and albumin/globulin ratio were used to assess liver function, pesticides decrease the total protein and albumin as a result of decrease synthesis of albumin in liver, and increase globulin (Barr et al., 2006). Altered liver enzyme activities have been reported among pesticide workers exposed to OP pesticides alone or in combination with organochlorine or other pesticides (Kamel et al., 2003).
The relatively elevated liver enzymes among exposed than controls elicited in the present study may reflect the hepatic effect of long term exposure to OP pesticides. This assumption was reflected on the chronic hepatocellular biochemical indicators, low protein and low albumin in the exposed than the control participants and could be documented by the statistically significant correlation between duration of exposure and both ALT and alkaline phosphatase. It may be due to that the effect of chronic exposure to pesticides that could result in acute or subacute liver insult (Deziel et al., 2015).
Liver injury would result in the delay or failure of the detoxification mechanisms with consequent earlier development of cumulative pesticide effects and hence a vicious cycle (Rani et al.; 2017). It may be emphasized that hepatic susceptibility to pesticides clinically and biochemically manifested to be mostly related to protein deprivation (Andreotti et al., 2009).
The oxidative damage of liver cells is promoted by exposure to OPs by enhancing peroxidation of membrane lipids marker changes in the overall histoarchitecture of liver in response to OPs,. This might be a result of toxic effects initiated by the production of reactive oxygen species causing destruction to the various membrane components of the cell (Mansour and Mossa, 2009).
The present significant increase in the mean measurements of blood urea and serum creatiine among the environmentally pesticides' exposed adolescent females (P<0.05, Table 5) agrees with that obtained by (Khan et al., 2005). Quandt et al., 2010 also found that among the 100 rice farmers in their sample, 23 farmers had abnormal levels of blood urea nitrogen (BUN), 22 of which had BUN values exceeding the upper boundary for the normal population. Similarly, Cavari et al., 2013 proposed that OP effects on the renal system could be due to direct parenchymal intoxication, secondary to hemodynamic instability or seizure-induced rhabdomyolysis (Yardan et al., 2013 and Mohamed et al., 2016).
On studying the hematological disorders among adolescent females environmentally exposed to pesticides, a statistically significant decrease in means of RBCs a, Hb and lymphocytes measurements was found among the exposed females in post exposure season (4.19±0.31 106/l, 12.322±0.65 gm∕dl and 2.98±0.68 103/dl; respectively) than either of the controls (4.82±0.42 106/l, 12.63±1.01 gm∕dl and 3.63±0.71 103/dl; respectively) or exposed in pre exposure season (4.71±0.37 106/l, 12.62±0.98 gm∕dl and 3.58±1.08 103/dl; respectively) (P< o.05, Table 6). Decreased RBCs count and hemoglobin may be attributed either to the fact that OP pesticides affect dietary intake (Leach, 2014) or due to the effect of pesticides on the bone marrow (Barr et al., 2006). Another possible mechanism is binding of organophosphate pesticides on iron, followed by a lack of incorporation of iron in hemoglobin (Abu Mourad, 2005).
Moreover, these results are in concordance with those of Mansour and Mossa, 2009 who revealed that most of the hematological, renal and liver indices were affected, where there were significantly lower values of RBC’s count, hemoglobin, lymphocytes count, total protein, albumin and A/G ratio in the exposed group (4.05 ± 0.24 ml/l, 12.37 ± 1.19 gm/dl, 2.35 ± 0.76 103/dl, 6.2 ± 0.88 gm/l, 3.45 ± 0.44 gm/dl and 1.56 ± 0.42; respectively) compared to the control group (4.78 ± 0.6 ml/l, 13.26 ± 1.04 gm/dl, 3.02 ± 0.86 103/dl, 7.54 ± 1.13 gm/l, 4.12 ± 0.5 gm/dl and 2.46 ± 0.9; respectively).
The relationship between the exposure to pesticides and decrement in the different spirometric measurements is confirmed by the presence of significant positive correlation of AChE levels with values of FVC%, FEV1%, FEV1/FVC%, FEF25-75% and PEF % (r = 0.62, 0.41, 0.55, 0.61 and 0.43; respectively) and (R2=0.231, 0.168, 0.302, 0.372 and 0.185)(P<0.05, Table 7). These results are consistent with the study of Chakraborty et al. (2009) who reported that in Indian agricultural workers the inhibition of AChE more than 50% was associated with increased reporting of respiratory symptoms and reduced lung function (13.6% lower mean FVC, and 15.6% lower mean FEV1) than non-agricultural workers..
As mentioned above, the current results showed a significantly lower level of AChE in the exposed adolescent females (238.49±23.83 IU/L) compared to the control ones (303.35±78.54 IU/L) (P<0.05, Fig. 1 – Table: 5). There are several studies that reported AChE level showing a consistent significant association between exposure to pesticides and AChE inhibition in farm workers. All studies stated that AChE was significantly lower in the exposed participants than the controls (Clayton et al., 2003, Abdel-Rasoul et al., 2008; and Khan et al., 2010). Jørs et al., 2006. reported a mean ChE activity of 7.11 kU/L for those who have sprayed with OPs compared to a mean ChE of 8.03 kU/L for those who have not and ChE activity of 8.03 kU/L for those who have not sprayed compared to a ChE activity of 7.60 kU/L for those who have sprayed from 1–3 times and a ChE activity of 7.12 kU/L for those who have sprayed >3 times. Moreover, there was a statistically significant negative correlation between levels of AChE and laboratory indices of SGPT (r=-0.27 and R2=0.073) and SGOT (r=-0.21 and R2=0.044) and a statidtically significant positive correlation with basophils' count (r=0.23 and R2=0.152) (P<0.05, Table 7), which means that there were significant liver effects in addition to clinical and biochemical changes significantly associated with lower levels of AChE (Jørs et al., 2006)
Limitations of the Study:
To the knowledge of the authors, there is a scanty number of studies and cohorts on the adolescent females environmentally exposed to pesticides. The obtained results could be more evidenced by the inclusion of additional studies.