Contaminants of Soil–Vegetable Interface

Contaminants of Soil–Vegetable Interface: History

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Subjects: Ecology

Contributor:

Rashmi Dubey

Vegetable consumption is considered as an important part of the human diet as it serves as an essential source of vitamins, nutrients, and minerals. In this regard, the demand for new technologies and ideas in the agricultural sector has grown steadily to help expand the production of vegetable crops. The uptake and accumulation of trace elements (TEs) and pharmaceuticals and personal care products (PPCPs) as contaminants in vegetables have been accelerated by man-made activities.

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1. Contaminants of Soil–Vegetable Interface

1.1. TEs

Vegetables contain essential minerals that comprise an important part of the human diet [21]. Minerals contain groups of metals and non-metals that play an important role in the growth and metabolism of plants. They can be categorized into macro/major or micro/trace elements [13]. Macro-elements, such as Ca, Mg, N, and P, are required in plants at high concentrations (>0.1% dry weight). In contrast, TEs are required in low amounts in plants and can be further subdivided into essential and non-essential TEs. Zn, Mo, Fe, Ni, B, Cr, and Cu are examples of essential TEs required for plant metabolism and development [22]. However, as the concentration of essential TEs exceeds 0.1% of dry weight, they can turn into toxic and harmful substances in the environment.

In contrast, non-essential TEs, such as Cd, As, Pb, and F, are not required for plant growth or development and are highly toxic. High concentrations of TEs can affect soil, plants, food crops, human health, and the surrounding environment in a negative manner [23]. TEs, such as Cd, Pb, As, Cu, and Cr, tend to exhibit high accumulation rates in the soil–vegetable interface. Such TEs are translocated in much greater amounts in plants and vegetables due to similar physio–chemical properties [24,25]. According to the United States Environmental Protection Agency, Pb is an extremely toxic metal present in the environment [26]. Noxious concentrations of Pb can inhibit the enzymatic activities of plants while decreasing the total protein content required for proper functioning in plant tissues [27]. Furthermore, Cd toxicity can decrease the seed germination process and affect the nutrient content in plants [28]. Pb and Cd can show intense mobility and translocation rates from the soil to plant roots [29,30]. In addition to Pb and Cd, As is also found predominantly in the environment and is carcinogenic in nature [31]. Increases in the concentration of As can result in the absence of seed germination, stunted growth, and a decrease in the dry weight of plants [32]. Moreover, Cu is known as an essential TE required for plant metabolic functions, such as counterbalancing redox reactions. However, Cu has shown a potential risk of toxicity in plants [33]. Excess Cu can induce reactive oxygen species (ROS) in plants and affect the photosystems in the photosynthesis process. Furthermore, Cu toxicity can lead to chlorosis and reduction of the total chlorophyll content in plants [34]. Likewise, Cr can decrease the biomass of plant cells, alter the soil-microbial population, and eliminate the nutrient assimilation process [35]. Cr can cause detrimental effects on the environment by accumulating easily even at low doses.

1.2. PPCPs

ECs can be defined as any chemicals or products of chemical origin used widely by humans. They are normally present in the environment at a low concentration range (ng L⁻¹ to µg L⁻¹), but can pose detrimental effects on living organisms. The accumulation of ECs in food crops has been studied under different (experimental/field) conditions [11,36,37]. The major ECs classes include PPCPs, pesticides, food preservatives, polyaromatic hydrocarbons, microplastics, and nanomaterials. In this section, we focus on the most prominent EC class found to have accumulated in vegetables, that is PPCPs. These ECs have shown significant uptake and translocation from soil to vegetable plants as documented in the literature [8,38,39]. PPCPs as mentioned above include pharmaceuticals and personal care products (PCPs). Pharmaceuticals are medicinal compounds of chemical origin used for the treatment and curing of diseases. Pharmaceutical drugs can inhibit soil microbial activity, soil respiration, seed germination, and the growth of plants [40]. They can target ion channels and may inhibit the transport of the essential enzymes and nutrients required for plant growth [12]. Li et al. [41] stated that pharmaceutical compounds can transfer into plants through contaminated soil. Pharmaceuticals include a broad range of products including antibiotics, cytostatic drugs, anti-inflammatory drugs, hormones, stimulant drugs (e.g., caffeine), β-blockers, and antiepileptic drugs. Antibiotics such as tetracycline, sulfadimidine, oxytetracycline, chloramphenicol, trimethoprim, tylosin, and erythromycin are biologically active compounds used for treating bacterial infections [10]. Anti-epileptic drugs such as carbamazepine, dilantin, and primidone, have also been widely reported in the environment due to their inordinate use. Carbamazepine is one of the most thoroughly investigated pharmaceutical drugs in plant uptake of PPCPs [42]. Furthermore, anti-inflammatory drugs including diclofenac, ibuprofen, naproxen, acetaminophen, and β-blockers such as atenolol and propranolol, have been found to have accumulated in vegetable plants [10].

Besides pharmaceuticals, PCPs include daily life and household items such as plasticizers widely used in plastic bottles, gels, shampoo, and other beautification/cosmetics products, synthetic musk including galaxolide used in fragrances, skin care products, preservatives (such as parabens), ultraviolet filters (such as oxybenzone), and antimicrobial products (such as triclosan and triclocarban) [43]. Triclosan can increase fungal diversity, decrease the soil respiration process, and reduce plant growth [44]. Triclosan and triclocarban are the most widely used PCPs that have been identified in plants and generally found in the concentration range of 10–40 mg kg⁻¹ [36]. The potential uptake of PPCPs through soil and vegetable plants has paved the way for its presence in humans.

2. Effect of TEs and PPCPs on the Growth of Vegetables

2.1. TEs

TEs can be accumulated in almost all vegetable parts including the root, stem, leaves, and tubers. It is reported that leaves tend to absorb a maximum amount of TEs followed by the root and stem [13]. TE toxicity can inhibit enzymatic activity and induce oxidative stress in the vegetables [115]. Pb and Cd can interfere and halt the transportation and absorption of other essential elements in vegetables, which can disrupt the photosynthesis process, electron transport chain, respiration rate, and growth in vegetables [116]. TE toxicity can also result in the reduction in leaf area, biomass, dry weight, shoot growth, and yield in vegetables [117]. Other prominent effects on the growth of vegetables includes an increase in oxidative and peroxidase enzymes along with a decrease in anti-oxidant activities [13]. TEs are independent and show different effects on different vegetables. For instance, it was found that Cd toxicity can alter root growth in potato and decrease protein content in carrot leaves [118] and can reduce fruit production in tomatoes [119]. Similarly, As can cause a reduction in photosynthetic pigments as reported for carrots, lettuces, and spinach [120]. Cr toxicity can impair seed germination and inhibit plant growth, can cause chlorosis in young leaves as investigated in onions, and induce nutrient imbalance and injury as studied in tomatoes [121]. In a study by Hamid et al. [122], it was found that Pb toxicity can increase the formation of the harmful chemical compound lead acetate in beans, and reduce chlorophyll content in peas. Similarly, TEs such as Cu may alter root development and inhibit the micronutrients activity [13].

2.2. PPCPs

The effect of PPCPs on vegetables depends on the specific class type of PPCPs, the concentration, and the vegetable species exposed [39]. The prominent effect on vegetables due to PPCP toxicity includes decreases in reproduction, reduction in root length, chlorosis, decreased biomass, increases in oxidative stress, and inhibition of growth [39,123]. For example, carbamazepine toxicity can result in burnt edges, decreased photosynthesis pigments, and white spots in vegetable plants [124]. The effect of industrial pharmaceuticals on the growth and germination of spinach through wastewater irrigation was studied by Islam et al. [125]. The results showed 92% germination rate in control conditions in contrast to PPCP contamination at only a 21% germination. Similarly, the roots and shoot length were significantly decreased in the PPCP-contaminated spinach. The authors concluded that PPCP contamination has deleterious effects on vegetables, which lowers the yield, growth, and biomass. Therefore, to avoid PPCP contamination, the proper treatment of effluent is critical before using it for irrigation. The effect of ten antibiotics was studied in carrots and lettuces to investigate their influence on seed germination and root and shoot length [126]. The results showed a negative impact on seed germination with a decrease in root vegetable growth. Goldstein et al. [127], stated that PPCPs such as carbamazepine have the maximum tendency to accumulate more in the leaves than in other parts of plants.

3. Health Risk through Consumption of Contaminated Vegetables

3.1. TEs

Consumption of contaminated vegetables can affect human health. The list of adverse effects on human health due to consumption of TE and PPCP-contaminated vegetables is presented in Table 5. Common symptoms due to TE toxicity on human health include mental retardation in children, malnutrition, central nervous disorders, decreased intra-uterine growth, dementia, insomnia, depression, liver and kidney disorders, weak immune systems, instability, decreased vision, gastrointestinal disorders, cancer, and death [13]. Regular exposure to Cd can lead to bronchiolitis, alveolitis, emphysema, and other respiratory diseases [128]. Certain neurological and mental illnesses can be induced especially in children due to Pb toxicity [129]. Moreover, Pb and Cd can readily accumulate in bone matrices and tissues and induce fractures and bone deformities. It can also cause malfunctioning of the lungs and liver and can affect other metabolic functions of the human body [49,130]. The toxicity range depends on the dietary intake of the contaminated vegetables and is assessed using health risk parameters. The various indices and parameters used in the assessment of the health risks posed by TEs and PPCPs is shown in Table 6. For TE-contaminated vegetables, the health risk assessment for humans is determined by parameters such as the daily intake of metals (DIM), hazard quotient (HQ), target hazard quotient (THQ), and health risk index (HRI) [13]. THQ measures the health risk posed by TEs through vegetable consumption. HRI represents the toxicity index, where a value <1 shows it is safe for the population and a value >1 shows detrimental effects on the population. For instance, a high HRI value was reported in a study on vegetables grown near Pb mines upon regular consumption of leafy vegetables. The risk assessment study revealed an HRI value >1 indicating a risk to consumers for several health problems, such as Alzheimer’s disease, due to excessive Pb intake through vegetables [129].

Table 5. Risk effects of TEs and PPCPs on human health.

S. No.	Contaminants	Health Risk Effect	References
A	TEs
1	Cd	Causes various types of cancer, prostate and breast cancer common, liver and kidneys most sensitive to Cd exposure, damage to hemopoietic system, rheumatoid arthritis, osteoarthritis, osteoporosis, renal and hepatic dysfunction, and pulmonary edema. Excess Cd can cause damage to lungs. It can induce neurodegenerative disease, affect male reproductive system, female menstrual cycle, impair reproductive hormones, fertility, pose a threat to the life of pregnant women and the newborn baby, and cause death.	[130,131,132]
2	As	Causes a variety of complications in the body’s organ system, such as the nervous, respiratory, cardiovascular, and integumentary systems, skin lesions, bone marrow depression, and encephalopathy. As is highly carcinogenic in nature causing various types of cancer including skin, bladder, lung, kidney, and liver cancer. Neurological disorders include intellectual function and memory loss, arsenicosis, diabetes, hypertension, hyperkeratosis, and melanosis.	[133,134]
3	Pb	Pb affects the central nervous system, cardiovascular system, and kidneys; pregnancy complications can occur, stopping fetal growth in the early stages of pregnancy, miscarriage in females, and male infertility; children have a high absorption capacity for Pb, it can pass through placenta causing birth defects, and can reduce maternal thyroid hormones. Pb can induce anemia, hypertension, renal dysfunction, neurotoxicity, heme synthesis, nephrotoxicity, and encephalopathy and can induce oxidative stress in the liver; excess Pb causes chronic respiratory and dermatogenic problems. It can act as substitute for Zn required in heme synthesis. It can cause various types of cancer due to its carcinogenic nature, leading to death	[129,135,136]
4	Cu	Affects liver and kidney failure through chronic or long-term exposure, diarrhea, headache, and mucosal irritation. High Cu concentrations can cause gastrointestinal disorders like jaundice, stomach pain, hematemesis, and vomiting. Other symptoms include hepatic necrosis, rhabdomyolysis, intravascular hemolysis, encephalopathy, depression, irritation, and mortality. Cu can also induce DNA damage due to oxidative stress	[137,138,139]
5	Cr	Chromosomal abnormalities, DNA strand breakage, risk of abortion or miscarriage, respiratory tract irritants can cause pulmonary sensitization, and the chronic inhalation of Cr (VI) causes risk of ulcers, lung or nasal cancer. Cr toxicity can induce stomach, kidney, bones, lungs, and other gastrointestinal disorders. It can impair broad spectrum alteration in DNA causing neoplasia	[13,140]
B	PPCPs	PPCPs have been detected in environmental entities due to their application as prophylactics, and growth promoters in food. Antibiotics distribution in vegetables have been found in the order of leaf > stem> root. Daily exposure to PPCPs can cause antibiotic resistance in humans which can increase the risk of death. Parabens suppress estrogen activity and induce an immediate hypersensitivity reaction. Many laboratory experiments have suggested a low risk of PPCPs exposure on human health. There still needs to be more field scale data under the current system of agricultural production for the analysis of PPCP toxicity on humans through the ingestion of contaminated vegetables.	[10,141]

Table 6. Toxicity assessment parameters for TEs and PPCPs.

S.No.	Parameters	Formula
A	TEs
1	Daily intake of metal (DIM)	DIM = A ∗ C ∗ D/B_W A = TEs concentration in plants (mg kg⁻¹) C = conversion factor D = daily intake of vegetable (kg day⁻¹) B_W = average human body weight (kg)
2	Hazard quotient (HQ)	HQ = (daily vegetable intake) ∗ (metal concentration in vegetable)/R_FD (oral reference dose in mg kg) ∗ body mass
3	Health risk index (HRI)	HRI = DIM/R_FD
4	Target hazard quotient (THQ)	THQ = 10⁻³ (E_F ∗ E_D ∗ F_IR ∗ C/R_FD ∗ W_AB ∗ T_A) E_F = exposure frequency (365 days year⁻¹) E_D = exposure duration (70 years) F_IR = food ingestion rate (g person⁻¹ day⁻¹) C = metal concentration in food (µg g⁻¹) R_FD = oral reference dose (mg kg⁻¹ day⁻¹) W_AB = average body weight (Kg) T_A = average exposure time for non-carcinogens
B	PPCPs
1	Estimated daily intake (EDI)	EDI = Daily intake rate (g person⁻¹ day⁻¹) ∗ PPCPs in vegetables (ng g⁻¹)/person average weight (kg person⁻¹)
2	Risk quotient (RQ)	RQ = EDI (ng Kg⁻¹ day⁻¹)/ADI (ng Kg⁻¹ day⁻¹)
3	Health hazard index (HHI)	$HI = \sum_{j = 1}^{n} R Q i$
4	Human exposure (HE)	HE = C ∗ D ∗ W ∗ T C-concentration of PPCPs in vegetables (ng/kg) D-average daily consumption of vegetables (Kg/day) W-human body weight (Kg) T-exposure time (day)

In addition, high levels of Cu exposure can cause anemia, and liver and kidney damage [137]. It is also associated with a genetic disorder called Wilson disease when it accumulates in the liver [142]. Cr in the form of Cr⁺⁶ is considered to be detrimental for human health due to its toxicity and carcinogenic nature [143]. Furthermore, Smith et al. [144] stated that the consumption of As-contaminated vegetables even at low concentrations can lead to irregularity in heartbeat, nausea, vomiting, and low red-blood cells (RBCs), and white-blood cells (WBCs) counts. In addition, high concentrations of As in vegetables can cause diabetes, cardiovascular disease, an increase in blood pressure, and neurological and pulmonary disorders as well as cancers when consumed regularly.

3.2. PPCPs

Imperceptible amounts of PPCPs in dietary intakes can cause allergies, especially in children. The health risks associated with the consumption of PPCP-contaminated vegetables are shown in Table 5. Long-term consumption of PPCP-contaminated vegetables, especially antibiotics, can lead to the development of resistance against natural human antibiotic activity, which can cause illnesses that are difficult to cure and can lead to death [109]. Likewise, Stuart et al. [43] reported in a review regarding the risk assessment of ECs that paraben toxicity can decrease estrogen activity and increase hypersensitivity reactions.

However, many laboratory studies have suggested a low risk of PPCPs on human health through vegetable consumption [7,10]. The annual human exposure value for PPCPs (i.e., carbamazepine, diclofenac, triclosan, and parabens) is acceptable in the range of 20–200 mg [10]. For instance, in a greenhouse experiment, a low annual exposure of PPCPs was reported for spinach in the range of 0.04 to 3.5 × 10² µg and for lettuce in the range of 0.08 to 1.5 × 10² µg for an average 70 kg individual [111]. These estimates in the study were much lower than the acceptable range (i.e., 20–200 mg) and showed a low risk of exposure through vegetable consumption. Similarly, triclosan exposure was found to cause minimal risk to human health in a study evaluating the health risk assessment [145]. To date, except for the laboratory-based calculations, there is not enough data under realistic field conditions to make conclusions for human safety regarding exposure to PPCPs via contaminated vegetable consumption [146]. Furthermore, the risks associated with PPC-contaminated vegetables are measured in terms of the risk quotient (RQ) and health hazard index (HHI) (refer to Table 6). RQ is defined as the ratio of the estimated daily intake (EDI) to the accepted daily intake (ADI) and HHI is calculated by the summation of the RQ of each of the PPCPs. When the RQ and HHI value is <0.01, PPCP-exposure risk to humans is negligible, while when the RQ and HHI value is >0.01 it shows the possibility of risk; when this value is >0.05 it shows a high risk for humans [10]. For example, in a study on the accumulation of pharmaceuticals in peanut kernels, their daily intake was explored with respect to their potential risks to human health [147].

This entry is adapted from the peer-reviewed paper 10.3390/su142114539

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